SEARCH · Search PubMed

Results for “Tuberculosis, Splenic”

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.

SourceResearch connectionFrom yearThrough year

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

At least 631 records · Page 35Linked to original sources

PubMed2002

Minilaparoscopy-guided spleen biopsy in systemic disease with splenomegaly of unknown origin.

With the advent of a minimally invasive laparoscopy technique, the advantages of diagnostic laparoscopy are being rediscovered. We report here on four patients with systemic disease of unknown origin and splenomegaly, in whom minilaparoscopy-guided splenic biopsy yielded a definitive diagnosis. Four patients with unclear systemic disease were studied using diagnostic minilaparoscopy and guided spleen biopsy, after failure of diagnostic work-up. Minilaparoscopic spleen biopsy revealed the diagnosis of a B-cell non-Hodgkin's lymphoma in two cases. In one patient, who had a history of Still's disease, the spleen biopsy showed granulocytic infiltration in the spleen typical of an acute episode of Still's disease. One patient with a known immunodeficiency syndrome (stage C III) showed multiple hypodense lesions in the spleen. Biopsy allowed a diagnosis of mycobacterial infection, with identification of Mycobacterium tuberculosis. No major complications occurred in any of the four cases; post-biopsy bleeding was observed in three of the four, but was easily managed by argon plasma coagulation or application of fibrin glue, or both. We recommend the use of spleen biopsy as a diagnostic tool in splenopathy of unknown origin if previous diagnostic methods have failed to yield a definitive diagnosis.

Acquired Immunodeficiency Syndrome↗

PubMed1995

Comparative assessment of metabolic enzyme levels in macrophage populations of the F344 rat.

The immune system is a direct target for toxic insult by a number of drugs and other chemicals, many of which require activation to toxic metabolites by drug-metabolizing enzymes. We compared the induction of drug-metabolizing enzymes, including cytochrome P450 1A1 (CYP1A1) and aldehyde dehydrogenase (ALDH), which are differentially expressed in various macrophage populations following treatment of F344 rats with the inducer 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Kupffer cells, alveolar macrophages and splenic macrophages from TCDD-treated animals expressed elevated levels of inducible CYP1A1 as compared to other macrophage subpopulations or cells from control rats. TCDD treatment also resulted in increased ethoxyresorufin-O-deethylase (EROD) activity and total cytochrome P450 content in tissue-derived macrophages. Immunoreactive protein and mRNA transcripts for CYP1A1 were not detectable in resident peritoneal macrophages or peripheral blood monocytes. Examination of aromatic hydrocarbon receptor (AhR) levels in macrophage populations suggests that the ability of TCDD to induce metabolic enzymes in specific cell types correlates well with AhR expression. In vivo activation of macrophages, using either Bacillus of Calmette and Guérin, Mycobacterium tuberculosis (BCG) or polyinosinic:polycytidylic acid (Poly I:C), caused no significant alteration in the levels of induction of CYP1A1. ALDH-3 induction was similar in all macrophage populations examined. These studies indicate that macrophages, particularly those from portals of entry, may be induced to produce increased levels of specific enzymes, and the induction is dependent upon their maturational stage rather than their activation state. The metabolism of xenobiotics to toxic intermediates by immune cells and its role in immunosuppression are discussed.

Aldehyde Dehydrogenase↗

PubMed2000

Protective role of interleukin-1 in mycobacterial infection in IL-1 alpha/beta double-knockout mice.

To understand the role of the proinflammatory cytokine interleukin-1 (IL-1) in mycobacterial inflammation, IL-1 alpha/beta double-knockout (KO) mice were produced. These mice were infected with either Mycobacterium tuberculosis H37Rv by the airborne route using an airborne infection apparatus, and their capacities to control mycobacterial growth, granuloma formation, cytokine, and nitric oxide (NO) production were examined. The IL-1 alpha/beta mice developed significantly larger (p < 0.01) granulomatous, but not necrotic, lesions in their lungs than wild-type (WT) mice after infection with H37Rv. Inflammatory lesions, but not granulomas, were observed in spleen and liver tissues from both IL-1 alpha/beta KO and wild-type mice. Granulomatous lesion development in IL-1 alpha/beta KO mice was not significantly inhibited by treatment with exogenous recombinant IL-1 alpha/beta. Compared with wild-type mice, splenic IFN-gamma and IL-12 levels were within the normal range. NO production by cultured alveolar macrophages from IL-1 alpha/beta KO mice was lower than in wild-type mice but were increased by the addition of recombinant IL-1 alpha/beta. Our data clearly indicate that IL-1 is important for the generation of early-phase protective immunity against mycobacterial infection.

Animals↗

PubMed2004

[Diagnosis of disseminated mycobacterial infection in AIDS patients by US-guided fine needle aspiration biopsy of lymphnodes and spleen].

Our aim was to evaluate the efficacy of abdominal US and fine-needle aspiration biopsy (FNAB) in the diagnosis of disseminated mycobacteriosis (DM) in patients with Acquired Immunodeficiency Syndrome (AIDS). We reviewed the US and clinical records of 18 AIDS patients (12 males; 22-43 years) with DM studied with abdominal US. 18 patients underwent fine-needle aspiration biopsy of enlarged abdominal lymphnodes and 11 underwent FNAB of the spleen. All aspirates were studied with acid-fast stain for fast examination and cultures for isolation of mycobacteria. Abdominal US showed: enlarged abdominal lymphnodes (diameter range: 5-35 mm; mean 17 mm) splenomegaly (spleen diameter range: 14-22 cm; mean: 16.2 cm) and hepatomegaly (right hepatic lobe thickness range: 14.5-18.5 cm) in all patients; multiple splenic abscesses (diameter range: 3-20 mm) in 11 patients; small intestine wall thickening in 5 patients (maximum bowel wall thickness range: 7-15 mm); mild to moderate ascites in 8 patients; pleural effusion in 4 patients; hyperechogenicity of the kidney cortex in 5 patients; peritoneal abscesses in one and a retroperitoneal abscess in one patient. fast-acid-stain of spleen and/or lymphnode FNAB specimens allowed early diagnosis of mycobateriosis in 18/18 cases (100%). Cultures of lymphnode aspirates grew mycobacteria in 10/18 patients (56%). Spleen aspirates grew mycobacteria in 11/11 patients (100%) Blood cultures were positive in 6/18 patients (33%). Diagnosis of species was M. tuberculosis in 9 and M. avium in 6 patients. In 3/18 patients (17%) all cultures were negative. In conclusion, abdominal US features suggest DM in AIDS patients. Spleen and/or lymphnode FNAB allows a specific diagnosis in 100% of the patients.

AIDS-Related Opportunistic Infections↗

PubMed1952

The inhibition by cortisone of the cytotoxic activity of PPD on tuberculin-hypersensitive cells in tissue culture.

Using the roller tube method of tissue culture, it has been shown that cortisone and compound F inhibit the cytotoxic action of PPD upon macrophages from the splenic tissue of tuberculous guinea pigs. Pretreatment of the cells for 24 hours with hormones before exposure to PPD was found to be essential. Estrone and desoxycorticosterone glucoside had no protective activity. Certain advantages of the tissue culture method in studies of tuberculin hypersensitivity and possible mechanisms and implications of this protective action of cortisone are discussed.

Animals↗

PubMed1993

Regulation of mycobacterial growth by the hypothalamus-pituitary-adrenal axis: differential responses of Mycobacterium bovis BCG-resistant and -susceptible mice.

The role of the hypothalamus-pituitary-adrenal (HPA) axis in regulating the growth of Mycobacterium avium in Mycobacterium bovis BCG-resistant and -susceptible congenic mice was evaluated. Restraint was used to activate the HPA axis, which resulted in an increase in the level of corticosterone in the plasma. Activation of the HPA axis increased the susceptibility of BALB/c.Bcgs mice to the growth of M. avium. In contrast, the growth of M. avium was not altered in BALB/c.Bcgr mice as a result of HPA activation. Adrenalectomy abolished the effect of HPA activation on mycobacterial growth, as did treatment of the mice with a glucocorticoid receptor antagonist, RU 486. Activation of the HPA axis also resulted in the increased susceptibility of splenic macrophages from Bcgs mice but not from Bcgr mice to M. avium growth in vitro. The production of tumor necrosis factor alpha and of reactive nitrogen intermediates by splenic macrophages from both strains of mice was suppressed as a result of HPA activation. The implications of these findings for resistance controlled by Bcg and for susceptibility to mycobacterial growth are discussed.

Adrenalectomy↗

PubMed1993

[Commemorative lecture of receiving Imamura Memorial Prize. Characterization of immunosuppressive macrophages induced in mice infected with Mycobacterium intracellulare].

Functional changes in T lymphocytes and macrophages (M phi s) in host mice during the course of Mycobacterium intracellulare infection were studied. In both strains of mice, BALB/c or C57BL/6 (susceptible to M. avium complex) and CBA/JN or C3H/He (resistant to M. avium complex), the smooth, opaque and dome-shaped colonial (SmD) variants of M. intracellulare were easily eliminated from the sites after week 2 of infection. In contrast, the smooth, transparent and irregularly shaped colonial (SmT) variants showed steady growth in the former strains of mice and persisted for long time even in the latter strains of mice. No difference was found between persistence of the organisms in euthymic (+/+) and athymic (nu/nu) BALB/c mice during the first 4 weeks after infection. Thereafter, more rapid growth was seen in the spleens and lungs of nu/nu mice. Thus, matured T cells may be important for the prevention of the progression of M. intracellulare infection to the terminal state. Next, the profiles of generation and characteristics of splenic M phi s which suppress the Con A mitogenic response of splenic T cells in host CBA/JN or BALB/c mice during the course of M. intracellulare infection were investigated. In M. intracellulare--infected mice, reduction in some cellular functions of host splenic T cells, such as the Con A mitogenic response and mixed leucocyte reaction, were seen around 2 weeks after infection, and this was accompanied by appearance of immunosuppressive M phi s in spleen cells (SPCs).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2004

The role of antigenic peptide in CD4+ T helper phenotype development in a T cell receptor transgenic model.

CD4+ Th1 cells play a critical role in the induction of cell-mediated immune responses that are important for the eradication of intracellular pathogens. Peptide-25 is the major Th1 epitope for Ag85B of Mycobacterium tuberculosis and is immunogenic in I-Ab mice. To elucidate the role of the TCR and IFN-gamma/IL-12 signals in Th1 induction, we generated TCR transgenic mice (P25 TCR-Tg) expressing TCR alpha- and beta-chains of Peptide-25-reactive cloned T cells and analyzed Th1 development of CD4+ T cells from P25 TCR-Tg. Naive CD4+ T cells from P25 TCR-Tg differentiate into both Th1 and Th2 cells upon stimulation with anti-CD3. Naive CD4+ T cells from P25 TCR-Tg preferentially develop Th1 cells upon Peptide-25 stimulation in the presence of I-Ab splenic antigen-presenting cells under neutral conditions. In contrast, a mutant of Peptide-25 can induce solely Th2 differentiation. Peptide-25-induced Th1 differentiation is observed even in the presence of anti-IFN-gamma and anti-IL-12. Furthermore, naive CD4+ T cells from STAT1 deficient P25 TCR-Tg also differentiate into Th1 cells upon Peptide-25 stimulation. Moreover, Peptide-25-loaded I-Ab-transfected Chinese hamster ovary cells induce Th1 differentiation of naive CD4+ T cells from P25 TCR-Tg in the absence of IFN-gamma or IL-12. These results imply that interaction between Peptide-25/I-Ab and TCR may primarily influence determination of the fate of naive CD4+ T cells in their differentiation towards the Th1 subset.

Animals↗

PubMed1976

In vitro studies on the mechanism of acquired resistance to tuberculous infection. I. The relationship between lymphocytes and macrophages in cellular immunity to tuberculous infection.

The relationship between lymphocytes and macrophages in cellular immunity against tuberculous infection was studied by means of an in vitro cell culture system without addition of streptomycin. The peritoneal macrophages were obtained from normal mice or mice immunized with heat-killed tubercle bacilli in paraffin oil, boosted with live BCG and infected with H37Rv cells in vitro. The infected monolayers of macrophages were cultivated for 48 hr with immune lymphoid cells obtained from immunized mice. The intracellular growth of H37Rv cells 3,5 and 7 days after infection was examined by counting tubercle bacilli within infected macrophages under a microscope. 1) The increase of bacilli within macrophages derived from immunized mice was slightly smaller than that in normal macrophages. 2) The addition of immune lymph node cells to the macrophage monolayers resulted in a marked decrease in the number of bacilli within both normal and "immune" macrophages. Conversely, normal lymph node cells exhibited an enhancing effect on the intracellular bacillary growth. 3) Immune lymph node cells showed a higher capacity to cause macrophages to suppress intracellular growth of bacilli than that of splenic lymphoid cells or thyrmocytes after addition to macrophage monolayers. 4) The treatment of lymphoid cells with inhibitors of protein synthesis, cycloheximide or streptovitacin A, resulted in a remarkable reduction of the ability of sensitized lymphocytes to cause macrophages to suppress multiplication of intracellular bacilli.

Animals↗

PubMedDate not supplied

[Tuberculosis in rheumatic patients treated with tumour necrosis factor alpha antagonists: the Portuguese experience].

In Portugal, 13 cases of tuberculosis (TB) were reported, in the period between 1999 and 2005, in 960 patients exposed to anti-TNFalpha treatment (1.35%), 8 females and 5 males. Mean age was 46.7 +/- 13.8 years. 9 patients had rheumatoid arthritis (RA), in 639 exposed patients (1.4%), 3 had ankylosing spondylitis (AS), in 200 exposed patients (1.5%) and 1 had psoriatic arthritis (PA), in 101 exposed patients (1%). The anti-TNFa used was in 8 cases infliximab (in 456 patients exposed, 1.5%), in 4 adalimumab (in 171 patients exposed, 2.3%) and in 1 etanercept (in 333 exposed, 0.3%). Treatment with a biological agent was started 11.1 +/- 8.7 months (min 3 and max 50) before TB onset. Tuberculin skin test (TST) was performed in 9 out of the 13 patients (the other 4 had started biological therapy before 2002). In 3 cases the TST response was 0 mm, in 3 less than 10 mm, in one was 14 mm and in two 20 mm. In the 3 cases with a TST response superior to 10 mm, isoniazid treatment 300 mg/d was prescribed, during 9 months. The time between first symptoms and TB diagnosis was 2.6 +/- 2.9 months. TB involvement was pulmonary in 6 patients, lymph node disease in 2, peritoneal and pulmonary in 2, osteoarticular in one case, lymph node disease and splenic in another and miliar TB in the last case. One death was reported; all of the other cases had a good outcome after anti-TB treatment. In two cases (one treated with adalimumab and the other with infliximab), paradoxical response to treatment occurred. None of the patients has restarted biological therapy after TB treatment.

Adult↗

PubMed1988

Pleiotropic effects of the Bcg gene. II. Genetic restriction of responses to mitogens and allogeneic targets.

The response of Bcgr and Bcgs spleen cells to allogeneic Ag, mitogens, and in a system of oxidative mitogenesis using neuraminidase and galactose oxidase was investigated in two Bcg congenic systems. The Bcgr macrophages supported the MLR across H-2 barrier much better than the Bcgs macrophages. At sub-optimal or optimal doses of mitogens Bcgr mice were higher responders than their Bcgs counterparts. The superior response of Bcgr spleen cells to Con A was further investigated with the aim of identifying the population expressing this phenotype. T cells of either Bcgr or Bcgs type showed equal ability to respond to Con A in the presence of macrophages. Purified splenic macrophages from Bcgr mice contained a significantly greater percentage of Ia+-bearing macrophages compared to Bcgs mice. Splenic macrophages of the Bcgr type were more efficient than their Bcgs counterparts at restoring the Con A response of accessory cell-depleted spleen cells. Resident peritoneal macrophages as well as splenic dendritic cells from Bcgr and Bcgs mice were equally efficient at restoring this response. Glutaraldehyde-fixed Bcgr splenic macrophages were shown to be more efficient than the Bcgs cells at replenishing the response of Con A-unresponsive spleen cells when supplemented with IL-1.

Animals↗

PubMed2000

Hemophagocytic syndrome.

This case report is about an elderly man who presented with a long-standing history of high-grade fever and weight loss. He initially had only hepatosplenomegaly, but then developed jaundice. He also had pancytopenia and raised liver enzymes. His septic screen was negative, but he had a positive Monospot test and immunoglobulin G for Epstein-Barr virus. The liver biopsy showed sinusoidal phagocytosis and the subsequent bone marrow aspiration and biopsy showed significant hemophagocytosis, hence Hemophagocytic syndrome was diagnosed. The fever was refractory to antibiotic and anti-tuberculosis therapy, but it responded only partially to steroids. Full response was only noticed following anti-viral treatment in the form of intravenous Ganciclovir. The patient's general condition, liver enzymes, bilirubin, hematological parameters and even the weight returned back to their normal range 2 weeks after Ganciclovir therapy. Cessation of this drug resulted in relapse of his symptoms and oral antivirals did not help. Splenectomy, steroid pulse therapy and immunosuppressive treatment were only partially helpful. Reintroduction of Ganciclovir did help for a short period. We conclude that our patient had virus-associated hemophagocytic syndrome most likely related to Epstein-Barr virus infection, which was then confirmed by the splenic biopsy, and that Ganciclovir can be of great help in eradicating the virus and treating the disease, provided that it is given for a long enough period.

Aged↗

PubMed2002

Anti-tumor mechanism of Z-100, an immunomodulatory Arabinomannan extracted from Mycobacterium tuberculosis strain Aoyama B, on pulmonary metastases of B16F10 melanoma: restoration of helper T cell responses via suppression of glucocorticoid-genesis.

In the present study, the anti-tumor mechanism of Z-100 was investigated with the use of pulmonary metastasis of B16F10 melanoma. In B16F10 mice, Th1 cytokine production (IL-2, IFN-gamma) was suppressed in comparison with normal mice. On the other hand, Th2 cytokine production (IL-4, IL-10) was increased in the B16F10 mice. The administration of Z-100 to B16F10 mice restored the balance of Th1/Th2 cell responses from the Th2 dominant state to the normal state. Z-100 significantly suppressed the pulmonary metastasis of B16F10 melanoma in a dose-dependent manner. These results suggest that Z-100 restored the breakdown of Th1 cell responses, resulting in the suppression of pulmonary metastasis of B16F10 melanoma. Moreover, Z-100 decreased the corticosterone levels, which is known to suppress the Th1 cell responses, in both serum specimens and splenic tissue, and the steroidogenic CYP11A1 mRNA expression in CD4+ T cells. These results suggest that a suppression of pulmonary metastasis and restoration of Thl/Th2 cell responses by Z-100 may be due to the decrease in the corticosterone levels and the steroidogenic CYP11A1 mRNA expression of CD4+ T cells in B16F10 mice. Further, the role of Th1 cytokine, IFN-gamma, on these activities of Z-100 was examined. The suppressive effects of Z-100 on pulmonary metastasis and restoration of Th1/Th2 cell responses were eliminated by the administration of anti-IFN-gamma mAb. Moreover, the suppressive effects of Z-100 on glucocorticoid-genesis were eliminated by the administration of anti-IFN-gamma-mAb. These results suggest that Z-100 restores the balance of Th1/Th2 cell responses via the suppression of glucocorticoid-genesis by Z-100-induced IFN-gamma. IFN-gamma acts as a key cytokine in anti-tumor activities of Z-100.

Adjuvants, Immunologic↗

PubMed1996

Disseminated BCG infection in severe combined immunodeficiency presenting with severe anaemia and associated with gross hypersplenism after bone marrow transplantation.

An infant with severe combined immunodeficiency (SCID) is described, who presented with severe anaemia and hepatosplenomegaly due to disseminated Bacillus Calmette-Guérin (BCG) infection involving the bone marrow, liver and spleen. After BMT, huge splenic enlargement occurred, presumably due to proliferation of engrafted donor lymphocytes, leading to severe hypersplenism. Peripheral blood cell consumption was resolved by splenectomy, but gradual loss of the marrow graft followed.

Anemia↗

PubMed2002

Mycobacterium avium infection of macrophages results in progressive suppression of interleukin-12 production in vitro and in vivo.

Interleukin-12 (IL-12) has been shown to have an important role in the host defense against Mycobacterium avium. We sought to determine if human monocyte-derived macrophages produce IL-12 upon M. avium infection. Although IL-12 can be measured in supernatants of M. avium-infected macrophages at 24, 48, and 72 h following infection, intracellular staining showed that 24 to 48 h after infection, IL-12 was synthesized chiefly by uninfected macrophages in the monolayer, suggesting that M. avium infection inhibits IL-12 production. In addition, the data also suggest that the longer macrophage monolayers were infected, the less IL-12 they were able to produce. Stimulation of macrophages with IFN-gamma prior to infection with M. avium resulted in greater production of IL-12 compared with unstimulated macrophages. Culture supernatant of M. avium-infected macrophage monolayers, but not control macrophages, partially inhibited IL-12 production by IFN-gamma-stimulated macrophages. This partial inhibition was not reversed by anti-interleukin-10 (anti-IL-10) and anti-transforming growth factor beta 1 (anti-TGF beta 1)-neutralizing antibodies. M. avium infection of macrophages in vitro also suppressed IL-12 synthesis induced by Listeria monocytogenes infection. Immunohistochemistry staining of spleen of infected mice showed that IL-12 production by splenic macrophages was more pronounced in the beginning of the infection but decreased later. Our data indicate that M. avium infection of macrophages suppresses IL-12 production by infected cells and that the suppression was not a result of the presence of IL-10 and TGF beta 1 in the culture supernatant.

Animals↗

PubMed1991

Susceptibility to infection with Mycobacterium avium is paradoxically correlated with increased synthesis of specific anti-bacterial antibodies.

A comparison was made between the levels of splenic and intestinal (Peyer's patches and thin intestinal epithelium) Ig production of C57BL/6 germ free and conventional C57BL/6, BALB/c, DBA/2 and C3H/He mice and the susceptibility to Mycobacterium avium infection, evaluated by the number of bacterial colony-forming units (CFU) found in the liver and in the spleen of the animals. Mice received an i.p. injection of either 5 x 10(6), 10(7) or 10(8) bacteria, or were given the larger inoculum intragastrically. Alternatively, mice were treated with an i.p. injection of M. avium bacterial sonicates. A marked increase of splenic IgA production, quantitatively associated with the size of the inoculum and thus with the degree of infection, was observed in susceptible compared to relatively resistant mice. This increase was observed at an earlier time following infection with the larger rather than with the smaller inocula. Consistent significant increases in splenic production of IgG isotypes were only observed in the susceptible mice after infection with the intermediate and larger inocula whereas a comparative increase of IgM was only clearly observed after infection with the larger inoculum. Intestinal Ig production remained unchanged, however, in both susceptible and relatively resistant mice after i.p. infection. Also, all mice were resistant to M. avium infection by the intragastric route and with this site of entry splenic and intestinal Ig production remained unchanged. Susceptibility to M. avium infection was also quantitatively associated with increased levels of circulating specific anti-bacterial antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Effects of the methanol extraction residue (MER) tubercle bacillus fraction on the production of antibodies in vitro. III. Consequence of prior sensitization to MER.

Mice repeatedly immunized with the methanol extraction residue fraction of tubercle bacilli (MER) in incomplete Freund's adjuvant produced high titers of circulating antibodies against MER, as assessed by the enzyme-linked immunosorbent assay (ELISA) method. Spleen cells derived from these animals failed to respond to the usual nonspecific immunopotentiating influence of MER on the primary production of antibodies (generation of specific plaque-forming cells) in vitro to sheep red blood cells. The defect was expressed by B lymphocytes and splenic macrophages, but not by splenic T lymphocytes or peritoneal exudate macrophagic cells. Impaired responsiveness by spleen cells from MER-immunized animals to nonspecific immunostimulation was also expressed with regard to another, unrelated biological response modifier, lipopolysaccharide. There was no impairment of responsiveness to polyclonal mitogenic stimulation. Possible mechanisms of the effects described are discussed.

Adjuvants, Immunologic↗

PubMed1986

Relationship of silica and bacillus Calmette-Guerin exposures to humoral and cellular immune functions.

The consequences of silica preexposures were studied on subsequent bacillus Calmette-Guerin (BCG) pulmonary infections. Silica had a variable effect on colonization by BCG depending on organ and number of BCG treatments. Silica preexposures resulted in increased numbers of free alveolar cells subsequent to BCG infections, with an initially rapid increase of neutrophils. Both silica and two BCG treatments were capable of decreasing the animals' splenic response to stimulations with Escherichia coli aerosols, and BCG greatly enhanced antibody-dependent cell-mediated cytotoxicity in silica preexposed mice. 5'-Nucleotidase activity was depressed by both silica and BCG in pulmonary washout cells indicating that inhalation of these substances may have a stimulating effect on the alveolar macrophages.

Animal Diseases↗