Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Granulomas”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMed1999

The clearance of tubercle bacilli & mycobacterial antigen vis a vis the granuloma in different organs of guinea pigs.

In the present study, an attempt was made to define the relationship of intact tubercle bacilli and/or their antigenic fragments to a granuloma in the guinea pig in order to distinguish an active from a resolving granuloma. In one set of animals, granuloma was induced in the skin by injecting heat-killed Mycobacterium tuberculosis intradermally and in another set, granuloma was produced in the lung and spleen by injecting live M. tuberculosis intramuscularly. The animals were sacrificed at various time points and skin, lung and spleen from the two groups were subjected to histological examination for the presence of granuloma, bacilli and antigenic fragments. In the dermal lesion, intact acid fast bacilli were cleared first by day 42 followed by the removal of their antigenic fragments by day 63 and finally by day 84, the granuloma had resolved completely. In the guinea pigs infected with live M. tuberculosis, removal of the bacilli followed by the clearance of antigen was observed. Though the granuloma itself did not subside completely in these animals, it was found that there was a reduction in congestion and oedema of the granulomatous area. It is concluded from the results that the demonstration of antigen at the site of lesion may be potentially useful to discriminate between a persisting and a resolving tuberculous granuloma.

Animals↗
PubMed2000

Different cytokines profiles in spleen cells and liver granuloma of Schistosoma mansoni experimentally infected mice during disease development.

To determine the importance of Th1 and Th2 cells in modulating granuloma formation, mRNA transcripts for Th1 (IL-2 and IFN-gamma) and Th2 (IL-4 and IL-5) cytokines were assessed by the molecular technique of in situ hybridization in the liver granuloma. The molecular studies showed few number of cells expressing mRNA transcripts for INF-gamma whereas, considerable number of IL-2 cells were present in the liver granuloma at 6 weeks post-infection (p.i.). Complete disappearance of IFN-gamma expressing cells were found when the disease progressed to 13 weeks p.i. Conversely, very high number of cells expressing mRNA transcripts for IL-4 and fair number of IL-5 cells were present at 7 weeks p.i. with a peak level of IL-4 cells at 13 weeks p.i. These in situ molecular studies of the liver tissues, demonstrated that Th1 cells were present at the very early granuloma development. Moreover, Th2 cells were required for its full development. The main interesting finding was the number of cells expressing mRNA for IL-4, as they were very huge and it might exceed the total number of lymphocytes per se in the granuloma. Lymphocytes from experimentally infected mice-spleen cells were also cultured in vitro with S. mansoni soluble egg antigen (SEA) and the same cytokines of lymphocyte supernatant were measured by ELISA assay. The levels of IFN-gamma and IL-2 were high to 6 wk. p.i. with a slight decline of IFN-gamma, and increasing amount of IL-2 at 10-13 wk p.i. Spleen lymphocytes of fully formed granuloma secreted high levels of IL-4 and IL-5. The results suggest that the development of schistosome egg-induced liver granuloma is a complex process and both Th1 and Th2 cell subsets sharing with other inflammatory cells (non lymphocytes), may play an important role in regulating and modulating the immuno-pathology of granuloma formation and the subsequent hepatic fibrosis.

Animals↗
PubMed2001

[Effects of anti-idiotypic antibody NP30 on modulation of egg granuloma formation and hepatic fibrosis of schistosomiasis].

OBJECTIVE: To study the effects of the monoclonal anti-idiotypic antibody NP30 active immunization on egg granuloma formation and hepatic fibrosis in Schistosoma japonicum infection. METHODS: ICR mice were actively immunized with NP30 100 micrograms x 3 i.p. every 10 days while the mice in control group were injected with SP2/0 ascites i.p. simultaneously. After cercariae challenging, the mice were killed at the 4th, 8th, 12th, 16th, 20th and 24th week, respectively. Mouse livers were removed and stained histochemically with VG and subjected to immunohistochemical assay of collagen type I, III and fibronectin(FN). The volume of egg granulomas and the content of collagen type I, III and FN were determined quantitatively by NYD-1000 Image Analysis System. RESULTS: The volume of egg granulomas in NP30 immunized group was much smaller than that of control group from the 12th week after cercariae challenge. The cellular components of egg granulomas in NP30 immunized group were significantly different from those of the control group, exhibiting two types of atypical egg granulomas were found. VG stain revealed that the average optical density of collagen in hepatic granulomas of experimental group was lower than that of control group. Immunohistochemical assay revealed that the contents of collagen type I, III and fibronectin in egg granulomas of experimental group were lower than those of control group. CONCLUSION: NP30 vaccination may induce both cellular and humoral protective immunity to modulate egg granulomas and suppress liver fibrosis of schistosomiasis japonica.

Animals↗
PubMed1992

Role of IL-4 and IFN-gamma in Schistosoma mansoni egg-induced hypersensitivity granuloma formation. Orchestration, relative contribution, and relationship to macrophage function.

A well defined model of T cell-mediated hypersensitivity-type granulomatous inflammation induced by Schistosoma mansoni eggs was used to assess the role of IL-4 and IFN-gamma in granuloma development. Synchronized pulmonary granulomas were induced and isolated from S. mansoni-infected mice during vigorous (8 wk) and modulated (20 wk) stages of the disease. The sequential production of IL-4 and IFN was determined and related to temporal changes in granuloma macrophage production of IL-1, TNF, and superoxide anion (O2-). During the vigorous stage, IL-4 was produced on days 1 and 2 of granuloma formation, whereas IFN was released in greatest amounts on days 4 to 8. The peak of IL-4 occurred in a window between the peak of IL-1 (1 day) and maximal TNF production (8 to 16 days). Maximal O2- release tended to parallel IFN production. During the modulated stage when the inflammatory response is attenuated, IL-4 production was dramatically reduced as were levels of IL-1 and TNF, but IFN production persisted and maximum O2(-)-producing capacity was only delayed in onset. mAb specific for IL-4 and IFN were used to examine the effect of in vivo depletion of these cytokines on granuloma development. Administration of a single 1.0-mg dose of anti-IL-4 antibodies to mice with synchronously developing granulomas dramatically reduced granuloma size (40 to 50% suppression of area) during an 8-day study period, whereas antibodies to IFN had no effect on size. However, the latter treatment reduced giant cell formation. Our results indicate that granuloma development involves an orchestrated production of cytokines possibly resulting from sequential participation of different Th cell populations. Moreover, IL-4 is a pivotal cytokine in anamnestic cellular recruitment and subject to endogenous regulation.

Animals↗
PubMed1992

Granuloma T lymphocytes in murine schistosomiasis mansoni have somatostatin receptors and respond to somatostatin with decreased IFN-gamma secretion.

The granulomas of mice infected with Schistosoma mansoni for 8 wk have macrophages that secrete somatostatin 1-14 (SOM). Within the granuloma, SOM has no known function. To uncover the possible significance of SOM produced within this granulomatous inflammation, we sought SOM receptors on distinct cellular components of the granuloma to identify cells targeted for SOM action. [125I]SOM 1-14 bound to dispersed granuloma inflammatory cells specifically and reversibly. Scatchard analysis suggested one receptor type (kDa 4.28 x 10(-9) M). Octreotide, a stable SOM derivative, displaced radioligand (kDa 1.01 x 10(-10) M), but SOM 1-28, substance P, and vasoactive intestinal peptide did not. The SOM receptor localized exclusively to a subset of granuloma CD4+ T lymphocytes. Using IL-5 and IFN-gamma ELISA, it was shown that granuloma T cells can secrete appreciable IL-5 and IFN-gamma when stimulated with Ag or mitogen. Both SOM and octreotide at concentrations as low as 10(-10) M substantially decreased IFN-gamma secretion from Ag or mitogen-stimulated T cells, but at concentrations as high as 10(-6) did not affect IL-5 production. Octreotide administered to animals in vivo decreased the intensity of the granulomatous response. Thus, some granuloma T cells have SOM 1-14 receptors. SOM 1-14, a product of granuloma macrophages, may participate in regulation of the granulomatous response by modulating the secretion of some lymphokines. Octreotide, a clinically useful SOM analog, mimics the action of SOM on the immune system.

Animals↗
PubMed1992

Suppurative granulomatous lymphadenitis. Immunohistochemical evidence for a B-cell-associated granuloma.

The cellular composition of suppurative granulomas was investigated by the application of monoclonal and polyclonal antibodies to paraffin sections and compared with nonsuppurative, hypersensitivity-type granulomas. Macrophages, T cells, and dendritic cells showed a similar distribution in both types of granulomas. In addition to the presence of granulocytes, a major difference between suppurative granulomas and hypersensitive-type granulomas concerned their relationship with B lymphocytes. Hypersensitive-type granulomas were surrounded by small mantle B cells, but they did not contain any B lymphocytes. In contrast, variable numbers of B cells were found either at the periphery or in the center of suppurative granulomas. In view of their morphology (medium size, pale cytoplasm, irregular nuclear shape) and phenotype (L26 +/LN1 -/MB2 +/MT2 +) these B lymphocytes closely resembled monocytoid B cells. The monocytoid B cells might have a role in the recruitment of polymorphonuclear granulocytes and in the development of the necrosis, which occur within suppurative granulomas.

Acid Phosphatase↗
PubMed1987

The role of an anti-idiotype antibody in regulating hapten (azobenzenearsonate)-specific granuloma formation.

Antibody regulation of hapten-specific granulomas was studied in mice in order to assess the relationship between an anti-idiotypic antibody and granuloma formation. An anti-idiotypic antibody was raised against the idiotype of an azobenzenearsonate (ABA)-specific antibody of A/J mice. The anti-idiotypic antibody was subcutaneously (s.c.) administered to syngeneic mice prior to challenge with ABA-coupled polyacrylamide beads injected into the intestinal wall. The results of such a challenge were assessed histologically for granuloma formation at 24-h intervals. Mice primed with anti-Id antibody and challenged with ABA-linked beads developed epithelioid granulomas at 72 and 96 hr post-challenge. Unprimed mice or mice primed with control antibodies did not develop granulomas when challenged with ABA-linked beads. Moreover, we found that priming with anti-Id antibody intravenously (i.v.) resulted in suppression of intestinal granuloma formation that was similar to that observed previously after priming mice i.v. with ABA-coupled spleen cells (Ginsburg et al., 1982). This study demonstrates the induction and suppression of hapten-specific granuloma formation in the intestine by an anti-Id antibody. The observations indicate a role for the idiotype-anti-idiotype interaction in regulation of hapten-specific granuloma formation, and may have implications for the manner in which the host reacts against self in the autoimmune inflammatory process.

Animals↗
PubMed1985

In vitro studies on dermal granulomas of human leprosy--cellular characteristics.

Single-cell suspensions from the granulomas of leprosy cases were prepared for an in vitro study of the properties of the infiltrating cells. Biopsies from 44 untreated patients with tuberculoid and lepromatous leprosy were analyzed. The granulomas were found to contain lymphocytes and "large cells" (epithelioid cells and macrophages). The number of lymphocytes was significantly higher in the suspensions from the tuberculoid granulomas in comparison to the suspensions from the lepromatous granulomas. A high percentage of lymphocytes from the tuberculoid granulomas formed rosettes with sheep erythrocytes, and also showed the presence of esterase as dots in the cytoplasm. However, the lymphocytes did not form rosettes with EAC. Most of the "large cells" from both types of granulomas were esterase positive, exhibited peroxidase activity, and did not carry receptors for C3. A high percentage of "large cells" in the tuberculoid granulomas was nonadherent to a plastic surface, while the lepromatous granulomas contained a high proportion of adherent "large cells."

Cell Adhesion↗
PubMed1994

Production of monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 alpha by inflammatory granuloma fibroblasts.

The formation of hepatic granulomas around persistently deposited Schistosoma mansoni eggs leads to parenchymal damage, ongoing fibrosis, and ultimate loss of liver function. In this study, the production of macrophage inflammatory protein-1 alpha (MIP-1) and monocyte chemoattractant protein-1 (MCP-1) by granuloma fibroblasts was examined to establish the potential contribution of intragranuloma fibroblasts to the maintenance of the chronic inflammation. Isolated fibroblasts from dispersed acute infection hepatic granulomas were grown in tissue culture for 3 to 4 weeks and used on the third or fourth passage. We initially surveyed fibroblasts for production of MIP-1 and MCP-1 by reverse transcription-polymerase chain reaction (RT-PCR) after stimulation with interleukin (IL)-1, tumor necrosis factor, interferon (IFN)-gamma, IL-4, or IL-10: cytokines found within the granuloma. These studies demonstrated constitutive expression of MCP-1 and differential up-regulation of MIP-1 on cytokine stimulation. Protein expression was then verified by immunohistochemical localization of MIP-1 and MCP-1 in paraformaldehyde-fixed fibroblasts and by direct quantitation of MIP-1 and MCP-1 in culture supernatants by specific ELISAs. These studies demonstrated constitutive expression of MCP-1 in unstimulated and cytokine-stimulated granuloma fibroblasts. In contrast, IL-1 (0.1 to 2.5 ng/ml), IFN-gamma (10 micrograms/ml), and IL-10 (2.5 to 10 ng/ml) were able to induce the significant production of MIP-1 by the granuloma fibroblasts. Interestingly, normal noninflammatory fibroblasts from uninfected mice showed no significant production of MIP-1 or MCP-1 in response to these cytokines. These results suggest that granuloma fibroblasts may be phenotypically altered compared with normal fibroblasts and have a significant role in leukocyte recruitment, granuloma growth, and maintenance of the egg-induced lesion.

Animals↗
PubMed1993

Granuloma eosinophils enhance IL-5 production by lymphocytes from mice infected with Schistosoma mansoni.

IL-5 is essential for granuloma eosinophilia in mice infection with schistosomiasis. The granulomas constitutively make IL-5 that originates from granuloma CD4+ T lymphocytes. This observation prompted us to learn whether non-T cell elements in the granuloma can promote constitutive IL-5 production. Neither granuloma eosinophils nor spleen cells from infected mice constitutively produced detectable levels of IL-5. Yet, mixing spleen cells with granuloma eosinophils resulted in spontaneous IL-5 secretion without promoting IL-4 production. Moreover, the admixed cultures were more responsive to anti-CD3 or soluble egg Ag than were cultures containing spleen cells alone. IL-5 ELISPOT assays in Transwell chambers showed that the cellular origin of IL-5 in the admixed cultures was the spleen cells, and that the phenomenon did not require cell-to-cell contact with granuloma eosinophils. Also, admixed cultures of granuloma eosinophils and spleen cells released less IL-5 in the presence of mAb that specifically blocked the biologic activity of either IL-2, IL-2R, or IAk. However, adding rIL-2 to spleen cell cultures at concentrations up to 100 U/ml could not stimulate secretion of IL-5. Because eosinophil supernatants contained no IL-2 as assessed by CTLL-2 bioassay, the release of IL-5 in response to eosinophils was not likely secondary to eosinophil secretion of IL-2. Thus, it appears that eosinophils produce a soluble substance that, with IL-2 and ongoing class II MHC/TCR interaction, enhances lymphocyte IL-5 output.

Animals↗
PubMed1996

Expression of inducible nitric oxide synthase in rat pulmonary Cryptococcus neoformans granulomas.

Rats, like humans, have extremely effective immune mechanisms for controlling pulmonary Cryptococcus neoformans infection. The mechanism(s) responsible for efficient immunity in rat experimental infection is unknown. Recently, induction of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) have been implicated as an important microbicidal mechanism by which activated macrophages effect cytotoxicity against microbes. In this report, we investigated the expression of iNOS in rat pulmonary cryptococcosis. Localization and regulation of NO production was studied by immunohistochemistry for iNOS in conjunction with immunohistochemistry for cell markers, cytokines, and cryptococcal capsular polysaccharide. iNOS immunoreactivity was detected in macrophages, neutrophils, vascular endothelium, and respiratory epithelium. Double-immunolabeling studies revealed that the most prominent iNOS immunoreactivity was localized to epithelioid macrophages (CD11b/c+) within granulomas; CD4+ and CD8+ T cells were numerous around granulomas but did not express iNOS. iNOS immunoreactivity was detected in a selective population of epithelioid macrophages within some granulomas but not others. iNOS- granulomas were identical to iNOS+ granulomas with respect to morphology and immunohistochemical profiles. Macrophage iNOS immunoreactivity was detected 1 week after infection in one out of four rats and was strongly expressed in all rats at 2 weeks (in up to 50 percent of the granulomas) but declined considerably by 25 days. iNOS expression coincided with granuloma formation and preceded a decrease in lung fungal burden, suggesting an anticryptococcal role for NO. By double labeling, cytokines that have been shown to promote (interferon-gamma, granulocyte/macrophage colony-stimulating factor) and inhibit (transforming growth factor-beta) macrophage iNOS expression were detected around iNOS+ granuloma. iNOS immunoreactivity was expressed in selected neutrophils (1 and 2 weeks) and endothelial cells (1 and 2 weeks and 25 days) in the inflamed lung. Airway iNOS immunoreactivity was limited to the luminal border of rare bronchiolar epithelial cells. iNOS immunoreactivity was not detected in uninfected rats. The present study provides the first evidence for association of iNOS expression with protective cellular responses to cryptococcal infection in vivo.

Animals↗
PubMed1996

Corynebacterium parvum- and Mycobacterium bovis bacillus Calmette-Guerin-induced granuloma formation is inhibited in TNF receptor I (TNF-RI) knockout mice and by treatment with soluble TNF-RI.

The aim of this study was to examine the role of TNF receptor I (TNF-RI) in the pathogenesis of heat-killed Corynebacterium parvum- and live bacillus Calmette-Guerin (BCG)-induced granulomas. Granuloma formation was analyzed in TNF-RI knockout mice and after treatment with soluble TNF-RI (sTNF-RI). TNF-RI knockout mice injected with C. parvum or BCG developed fewer and smaller granulomas than wild-type control mice. Mice treated with sTNF-RI from days 7 to 13 after injection of C. parvum or BCG developed fewer and smaller granulomas than saline-treated control mice. Established granulomas regressed in rats treated with sTNF-RI from days 10 to 13 after injection of C. parvum. In conclusion, TNF signaling via TNF-RI contributes to the pathogenesis of C. parvum- and BCG-induced granulomas. sTNF-RI inhibits the development of granulomas and can cause the regression of established granulomas.

Animals↗
PubMed1997

Schistosome egg granulomas and hepatic expression of TNF-alpha are dependent on immune priming during parasite maturation.

Granulomatous inflammation is key to the pathogenesis of many infectious diseases, including hepatic schistosomiasis. The granulomas that form around schistosome eggs trapped in the liver of infected hosts were thought to be induced primarily, if not exclusively, by egg Ags. We now show that the maturation of adult worms, before the production of eggs, primes local immune responses key to granuloma formation. When parasite eggs are injected into the livers of naive animals, only a minimal, nongranulomatous, inflammatory response results. However, if eggs are injected into the livers of mice previously infected with single-sex adult worms, granuloma formation is restored. Granuloma formation is also restored if mice are presensitized with adult worm homogenates or with eggs themselves before egg injection into the liver. These sensitization studies confirm that an Ag or Ags are shared between different stages of the schistosome life cycle and that immune priming by these Ag(s) is necessary for hepatic granuloma formation. Models of infection that isolate the effects of worms from those of eggs confirm that each of these life cycle stages induces a unique pattern of cytokine expression. Hepatic expression of TNF-alpha, a major cytokine signal for granuloma formation, is a reaction to adult worms, not eggs. TNF-alpha may mediate immune priming necessary for granuloma development since injection of purified TNF-alpha alone restores formation of granulomas in the livers of naive mice injected with eggs.

Animals↗
PubMed1997

Neutrophils and reactive oxygen intermediates mediate glucan-induced pulmonary granuloma formation through the local induction of monocyte chemoattractant protein-1.

Monocyte chemoattractant protein-1 (MCP-1), which is required for full development of glucan-induced granulomas, in the rat, is expressed in the walls of blood vessels at sites of glucan embolization. Early (1 hour) vessel wall expression of MCP-1 is temporally and anatomically linked to the transient accumulation of neutrophils, even though these cells are not present within definitive lesions. To ascertain the potential pathophysiologic role of neutrophils in glucan-induced granuloma formation, rats were neutrophil-depleted using specific antiserum. There was a marked reduction in mean granuloma size and number in neutrophil-depleted animals when compared with neutrophil-sufficient controls. To determine potential mechanisms through which neutrophils may participate in granuloma formation, the antioxidant enzymes superoxide dismutase and catalase were administered to neutrophil-sufficient animals that had received glucan. Superoxide dismutase treatment did not reduce granuloma formation, whereas catalase treatment resulted in decreased granuloma size, suggesting that H2O2 plays an important role in this process. The local expression of MCP-1 mRNA and protein, as determined by in situ hybridization and immunohistochemical analysis, respectively, was decreased in both neutrophil-depleted and catalase-treated animals but not in superoxide dismutase-treated rats. Quiescent human umbilical vein endothelial cells incubated with either H2O2 or activated neutrophils secreted MCP-1. These data indicate that neutrophils and H2O2 are required for both full granuloma development and early blood vessel wall-associated MCP-1 expression after glucan infusion. These in vivo data, coupled with in vitro data that indicate that both catalase-sensitive reagent H2O2 and neutrophil-derived reactive oxygen intermediates (ie, H2O2) can induce MCP-1 secretion by human umbilical vein endothelial cells, support the hypothesis that neutrophils and neutrophil-derived products (H2O2) influence granuloma formation through induction of local MCP-1 expression.

Animals↗
PubMed1997

Immunohistochemical and ultrastructural analyses of in situ activation of hepatic stellate cells around Propionibacterium acnes-induced granulomas in the rat liver.

Stellate cells embrace the hepatic sinusoids as pericytes. To demonstrate their activation in juxta-sinusoidal location, we induced hepatic granulomatous inflammation, which did not accompany liver injury nor fibrosis, by administrating a low dose (10 mg/kg b.w.) of heat-killed Propionibacterium acnes into rats. Macrophages and lymphocytes migrated out of the sinusoid and made compact granulomas in the space of Disse. Stellate cells which faced on the granulomas were closely attached to the sinusoidal endothelial cells and extended projections into the spaces between the constituent mononuclear cells of granulomas. They did not migrate into granulomas nor displayed mitosis. Immunohistochemically, stellate cells around the granulomas expressed alpha-smooth muscle actin (alpha-SMA), whereas those in the non-granulomatous regions did not. Small deposits of type III collagen were found at the periphery of granulomas. Biochemical analysis showed an increased amount of alpha-SMA protein and type III collagen mRNA in the granuloma-bearing liver. Transforming growth factor-beta and platelet-derived growth factor were detected within the granulomas. The present study has revealed that stellate cells are activated in situ by extrasinusoidal macrophages in a paracrine manner without being detached from the sinusoidal wall.

Animals↗
PubMed2000

Severe episodic headache as the sole presenting ictal event in patients with a solitary cysticercus granuloma.

OBJECTIVES: Most patients with a solitary cysticercus granuloma present with seizures and severe episodic headache as the sole presenting symptom is rare in these patients. We report the clinical features, evolution and outcome of the disease in patients with a solitary cysticercus granuloma who had severe headache alone without seizures as the sole presenting event. MATERIAL AND METHODS: This was a prospective study which included all patients who presented with severe episodic headache alone and had a diagnosis of a solitary cysticercus granuloma based on CT imaging and follow-up and were managed in our department between June 1, 1991 and May 31, 1998. RESULTS: Out of nearly 550 patients diagnosed to have a solitary cysticercus granuloma during the period of the study, 15 patients (2.5%) presented with severe episodic headache alone. While 9 patients had 1 episode of headache, 6 patients had 2 to 5 episodes. Patients were managed with conservative symptomatic therapy (13 patients) and albendazole therapy (2 patients). Follow-up scans showed complete or partial resolution of the granuloma in 8 patients and a lesion of the same size in 4 patients. None of the patients with complete resolution of the granuloma reported further episodes of headache. CONCLUSIONS: It is important to recognize this presentation of a solitary cysticercus granuloma as it could be confused clinically with other acute central nervous system illnesses such as subarachnoid haemorrhage and meningitis. In regions endemic for cysticercosis a contrast enhanced CT scan of the brain should be performed in patients presenting with sudden onset of severe headache when a plain scan does not reveal intracranial haemorrhage as only a contrast enhanced scan will reveal the granuloma.

Adolescent↗
PubMed2001

Tuberculous granulomas in childhood tuberculous meningitis: radiological features and course.

The clinical course and serial cranial computerized tomographic (CT) findings of 202 children with tuberculous meningitis (TBM) admitted to Tygerberg Hospital between 1985 and 1994 were reviewed with regard to the incidence, CT appearance and clinical course of associated intracranial tuberculous granulomas. Thirty-four patients (16.85 per cent) had associated intracranial granulomas. Thirty-eight individual lesions were analysed and classified as meningeal, parenchymal or ependymal according to their central nervous system (CNS) location. Twenty-five patients had round to irregular, brain iso-, hypo- or hyperdense meningeal granulomas with variable degrees of enhancement and peri-lesional hypodensities. Four patients had diffusely enhancing, brain isodense, enplaque-like ependymal granulomas associated with the ventricular ependymal lining. Four patients with miliary tuberculosis and TBM showed multiple small diffusely enhancing, brain iso- or hyperdense parenchymal lesions and associated hypodensities on initial CT. Although granulomas in the meningeal and ependymal group had the propensity to paradoxically enlarge or appear on standard four-drug antituberculosis therapy, the majority resolved uneventfully. Rapid resolution of small parenchymal granulomas associated with miliary tuberculosis occurred in all cases. Most granulomas in this series were co-incidental, asymptomatic CT findings. In rare cases, the development or enlargement of a strategically located granuloma may result in complications.

Child↗
PubMed1992

Nonviable autologous bronchoalveolar lavage cell preparations induce intradermal epithelioid cell granulomas in sarcoidosis patients.

Intracutaneous injection of sarcoidosis patients with Kveim-Siltzbach antigen (KSAg), a particulate suspension of granulomatous sarcoidal spleen, induces an influx of T-helper lymphocytes and monocyte-macrophages followed by epithelioid cell granuloma formation. In the lung, similar granulomas form from an alveolitis of similar mononuclear cells, which may harbor a Kveim-like granulomagenic factor. To assess this possibility, preparations of nonviable autologous bronchoalveolar lavage cells (NABC) and KSAg were injected intracutaneously at different sites and biopsied at 4 to 5 wk. Of 22 sarcoidosis patients, nine (41%) developed typical granulomas at the NABC site, while all developed granulomas at the KSAg site. Responders to NABC had more recent onset of symptoms than nonresponders (3.2 versus 23.7 months, p less than 0.01), but did not have significantly higher percentages of lavage lymphocytes or more rosetting of lymphocytes about alveolar macrophages. None of 11 normal volunteers developed granulomas in response to NABC. Epithelioid cell granulomas at NABC and KSAg sites were similar by hematoxylin-eosin staining and by biotin-avidin-peroxidase immunohistochemical staining with monoclonal antibodies Leu-1, Leu-14, Leu-2a, Leu-3a, anti-interleukin-2 receptor, and polyclonal antibodies against lysozyme and alpha 1-anti-chymotrypsin. Symptomatic onset of sarcoidosis is associated with an autologous lavage cell factor that induces intradermal epithelioid cell granulomas that are immunophenotypically similar to Kveim-induced granulomas.

Adult↗