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PubMed1988

[Effect of prolactin on the enzymatic activity of thyroid follicular cells during stress due to surgery and subsequent subcutaneous inflammation].

In order to reveal prolactin (Prl) effect on the enzymatic activity of the thyroid follicular cells at a subcutaneous inflammation, 2 series of experiments have been performed on 100 non-inbred male rats with body mass of 150-170 g. In order to produce the inflammation, under ether narcosis celloidin globules are introduced subcutaneously in the abdominal wall. The test animals are given 0.125 mg of "Lactin" (the Soviet preparation of bovine Prl) in 0.5 ml of isotonic solution once every day, beginning immediately after the operation. At the same time the control animals are given 0.5 ml of isotonic solution. The time of observations are--2, 12 h, 1, 2, 3, 5, 10, 15 days after the operation. As a result of quantitative cytochemical investigation of the enzymatic activity in the thyroid follicular cell, multiphasic dynamics of SDG, LDG, G-6-PhDG, NADH-DG, NADPhH-DG, MAO activity and changes in carbohydrate metabolism type at various time of the subcutaneous inflammation are revealed. Daily injections of Prl against the background of the inflammation reduce amplitude of fluctuations of the enzymatic activity in thyrocytes. At late stages of inflammation (up to 2 days) Prl slows down the decrease of SDG, G-6-PhDG, NADH-DG, NADPhH-DG activity and accelerates decrease of LDH activity. At early stages of inflammation (3-15) Prl slows down decrease of NADPhH-DG, NADH-DG activity and decreases LDH and NADH-DG activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

[Effect of vitamin E on experimental inflammation in rats].

Besides other mediators like prostaglandins, kinins and histamine, oxygen radicals potentiate inflammations. Vitamin E as natural antioxidant could scavenge radicals produced during an inflammation and therefore reduce the inflammatory response. In experiments with male Wistar rats maintained on a diet deficient in or supplemented with vitamin E for 6 weeks the influence of the administration of DL-alpha-tocopherol on the inflammation of the right hind paw was tested. The irritation produced by injection of Freund's complete adjuvants was observed for 21 days. Measuring the thickness of the paw and the activity of acid phosphatase in the paw tissue there was no difference in the intensity of inflammation among the control and the vitamin-E-deficient diet groups. The supplementation with a pharmacological dose of tocopherol (324 mg DL-alpha-tocopherol/100 g food) had no effect on the inflammation of animals with different vitamin E supplements. Differences in the antioxidant status (contents of tocopherol and malondialdehyde in several organs, activity of creatine kinase in plasma) among the groups were mainly linked to the various tocopherol supplies. The irritation increased the lipid peroxidation in liver mitochondria and the activity of creatine kinase in the plasma. The data show no influence of vitamin E on this kind of inflammation.

Acid Phosphatase↗
PubMedDate not supplied

Heat, cold and inflammation.

Although therapeutic heat and cold measures are widely used in rheumatic diseases, their application in joint inflammations is still broadly empirical. Animal experiments concerning the effects of systemic hyperthermia and of local heat and cold applications upon experimentally induced inflammations (dextran edema, formol edema, kaolin edema, carrageenan edema, adjuvant arthritis) show that some inflammations are significantly depressed, i.e. they are effected by a useful therapeutic influence, but that cold and heat can also act as enhancing inflammatory stimulus. Under certain conditions, whole-body hyperthermia has immuno-suppressive effects. Although the exact points of intervention of heat and cold investigations, acute exsudative inflammations seem to be better influenced by cold; on the contrary, chronic torpid and proliferous inflammations are better influenced by heat. Prostaglandin mediated inflammations can be aggravated by cold, because it stimulates the prostaglandin synthesis; acute exsudative inflammatory processes are most often aggravated by heat. These results show that both therapeutic agents should be applied within a well-defined range and with care.

Animals↗
PubMed1994

Inflammation is responsible for the development of wound-induced tumors in chickens infected with Rous sarcoma virus.

When newly hatched chicks are given injections of Rous sarcoma virus, a tumor develops at the site of injection. In spite of the presence of the virus in the blood, no other tumors are found distant from the site of inoculation during the life span of the animal (4-6 weeks). However, if a wound is made away from the primary tumor, a tumor develops at the site of wounding. Work in our laboratory showed previously that these wound tumors do not develop as a result of metastasis, therefore, factors released upon wounding must contribute to the development of the wound tumors. In particular, we showed that transforming growth factor (TGF) beta, a growth factor implicated in wound healing, can replace wounding in tumor development. However, we also showed that epidermal growth factor and TGF-alpha, growth factors that also have roles in wound healing, do not induce tumors. To identify the critical event(s) and to determine the mechanism involved in wound tumor development, we have continued these studies. Here we show that: (a) wound tumor development correlates with the presence of circulating virus and inflammation; (b) the virus is present in serum and in heterophils of the peripheral blood; (c) cell division at the site of wounding precedes the expression of viral proteins; (d) in addition to TGF-beta, acidic and basic fibroblast growth factors can also replace wounding in tumor development; (e) these three factors (TGF-beta, acidic fibroblast growth factor, basic fibroblast growth factor) which promote tumors also induce inflammation, whereas epidermal growth factor and TGF-alpha do not; and (f) during the inflammatory response, blood vessel leakage occurs as tested by the release of fibrinogen into the tissues. To test the possibility that inflammation is the key element in the development of these wound tumors, we used beta-methylprednisolone, an antiinflammatory drug that inhibits inflammation (including blood vessel leakage), to determine if wound tumor development could be prevented. We found that when inflammation was inhibited, tumors were also inhibited; when inflammation could not be stopped, tumors developed as before. These results indicate that the effect of wounding on the development of wound tumors in Rous sarcoma virus-infected chicks is accomplished through the cytokines released by the inflammatory cells at the site of wounding. These inflammatory mediators play a critical role in providing the conducive environment for oncogene integration and activation, and subsequent development of tumors.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Periductal inflammation and cigarette smoke.

BACKGROUND: Cigarette smoking has been implicated in the etiology of periductal mastitis. The mechanism by which it causes inflammation around the mammary ducts is unknown. STUDY DESIGN: Inflammation and dilatation of the mammary ducts were compared in two groups of women with proven histologic diagnoses of periductal mastitis (PDM, n = 133) and intraductal papilloma (IDP, n = 98) over an eight year period. This study was done to determine if the number of cigarettes smoked correlated with the amount of periductal inflammation seen in PDM. Duct dilatation, periductal inflammation, and squamous metaplasia were assessed objectively by two pathologists without knowledge of the clinical parameters. RESULTS: Women with PDM were significantly more likely to be smokers than women with IDP (p < 0.001). Women with severe periductal inflammation were more likely to be younger (p < 0.05) whereas those with duct dilatation were more likely to be older (p < 0.02). Women with PDM who were heavy smokers (more than ten cigarettes per day) had more periductal inflammation (p = 0.0006) and squamous metaplasia of the lactiferous ducts (p < 0.02) compared with light or nonsmokers. Duct dilatation did not correlate with smoking habits. CONCLUSIONS: Cigarette smoking appears to be an important etiologic factor in periductal mastitis and appears to have direct toxic effects on the mammary ducts.

Adult↗
PubMed1998

IL-10 regulates thrombus-induced vein wall inflammation and thrombosis.

Vein wall inflammation associated with venous thrombosis is mediated by an imbalance in proinflammatory as compared with antiinflammatory molecules. We hypothesize that IL-10 is an important antiinflammatory cytokine that influences vein wall inflammation and thrombus propagation during venous thrombosis. To test this hypothesis a model of inferior vena caval thrombosis was used. Studies were performed at sacrifice 2 days after thrombus induction and included leukocyte morphometrics, myeloperoxidase activity, vein wall permeability, thrombus weight, and IL-10 ELISA analysis from the vein wall. IL-10 was elevated in the vein wall during venous thrombosis. Neutralization of IL-10 increased inflammation, while supplementation with rIL-10 demonstrated a dose- and time-dependent decrease in inflammation. Interestingly, a low 2.5-microg rIL-10 dose given at time of initiation of thrombosis most significantly decreased inflammation. Thrombus weight was importantly diminished by reconstitution of IL-10. These studies support an important role for IL-10 in the regulation of thrombus-associated inflammation and thrombosis and suggest that IL-10 could be used as a therapeutic agent in the treatment of venous thrombosis.

Animals↗
PubMedDate not supplied

The role of neutrophils in inflammation.

It has long been noted that inflammation underlies asthma. It is now recognized that there is marked heterogeneity in the stimuli that can cause or aggravate this inflammation, the cells that are involved in the response and the consequences in terms of both pathology and symptoms. The prime role of eosinophilic inflammation in the pathogenesis of asthma is acknowledged in this paper, but the potential role of neutrophilic inflammation to underlie symptoms and physiological changes that are characteristic of asthma is highlighted. A minority group of patients appear to have asthma from clinical signs, but their airway secretions do not contain eosinophils. Their response to treatment is unlike that of patients with typical eosinophilic airway inflammation in that they do not respond to steroid therapy. Published data from in vitro and animal work provide a conceptual framework to explain these observations. The refinement of the technique of examining sputum cellular content to assess airway inflammation provides an opportunity to identify and study this subgroup of patients.

Adult↗
PubMed1998

Activation of CNS circuits producing a neurogenic cystitis: evidence for centrally induced peripheral inflammation.

We present a model of neurogenic cystitis induced by viral infection of specific neuronal circuits of the rat CNS. Retrograde infection by pseudorabies virus (PRV) of neuronal populations neighboring those that innervate the bladder consistently led to a localized immune response in the CNS and bladder inflammation. Infection of bladder circuits themselves or of circuits distant from these rarely produced cystitis. Absence of virus in bladder and urine ruled out an infectious cystitis. Total denervation of the bladder, selective C-fiber deafferentation, or bladder sympathectomy prevented cystitis without affecting the CNS disease, indicating a neurogenic component to the inflammation. The integrity of central bladder-related circuits is necessary for the appearance of bladder inflammation, because only CNS lesions affecting bladder circuits, i.e., bilateral dorsolateral or ventrolateral funiculectomy, as well as bilateral lesions of Barrington's nucleus/locus coeruleus area, prevented bladder inflammation. The close proximity in the CNS of noninfected visceral circuits to infected somatic neurons would thus permit a bystander effect, leading to activation of the sensory and autonomic circuits innervating the bladder and resulting in a neurogenic inflammation localized to the bladder. The present study indicates that CNS dysfunction can bring about a peripheral inflammation.

Animals↗
PubMed1976

[Inflammation of the tail in swine. Slaughter-house findings during 1972, 1973, and 1974 (author's transl)].

In the Public Salughter-House of Utrecht, a percentage increase in the number of pigs with inflammation of the tail, which had or had not healed, was observed during the period from 1972 to 1974 inclusive. The most common secondary symptoms of inflammation consisted in embolic pneumonia, osteomyelitis of the vertebrae and abscess formation in other parts of the body, particularly the semimebranosus muscles. Osteomyelitis was found to be the most common complication in pigs in which the inflammation of the tail had healed, whereas this usually consisted in embolic pneumonia in those cases in which the inflammation of the tail had not healed. The bacteriological examination carried out in accordance with the Meat Inspection Regulations was positive in 21.7 per cent, 13.5 per cent of the cases respectively in 1972, 1973 and 1974. Micro-organisms were isolated much more frequently from the kidney than they were from the spleen and meat. There was no relationship between the presence of inflammation of the tail and climatological conditions during the fattening period. The losses at slaughter from inflammation of the tail in the Netherlands are estimated at 3-4 million guilders per annum.

Animals↗
PubMed2003

Idiopathic orbital inflammation: distribution, clinical features, and treatment outcome.

OBJECTIVE: To evaluate the distribution and clinical as well as treatment outcome characteristics of idiopathic orbital inflammation with the aim of delineating a more systematic approach to diagnosis and treatment. METHODS: A 10-year retrospective review of patients with idiopathic orbital inflammation treated at one institution. RESULTS: Ninety eyes in 65 patients (22 men and 43 women) were studied. Diagnoses were isolated dacryoadenitis (n = 21), isolated myositis (n = 19), concurrent dacryoadenitis and myositis (n = 5), orbital apex syndrome (n = 6), and idiopathic inflammation involving the preseptal region, supraorbital region, sclera, Tenon capsule, orbital fat, or optic nerve (n = 14). The mean age at presentation was 45 years. Pain and periorbital swelling were the most common clinical features and were observed in 45 (69%) and 49 (75%) patients, respectively. Seventeen patients (26%) had bilateral involvement. Biopsy was performed in 19 patients (29%) with atypical presentations or who failed to respond to the initial therapy. Patients were treated with steroids alone (n = 45), steroids and subsequent radiation therapy (n = 8), steroids and nonsteroidal anti-inflammatory agents (n = 6), nonsteroidal anti-inflammatory agents alone in mild cases (n = 2), and, rarely, radiation therapy without steroids (n = 1) or surgical debulking alone (n = 1). Of 65 patients, 41 (63%) represented treatment successes, with complete symptom relief at the time of the last follow-up, and 24 (37%) represented treatment failures, with partial or no relief of symptoms. Treatment failures were often characterized by recurrence of inflammation after a period of quiescence (58%) and unremitting, recalcitrant inflammation (38%); 1 patient ultimately required an exenteration. CONCLUSION: Systemic steroid with a slow taper has been the established first-line treatment for idiopathic orbital inflammation, but refractory cases accounted for a significant portion of treatment failures in our study, reflecting the need for a more systematic approach to the study of this multifaceted disease and for therapeutic alternatives to systemic steroids.

Adolescent↗
PubMed2003

Alterations in corneal stromal dendritic cell phenotype and distribution in inflammation.

BACKGROUND: The normal corneal stroma is endowed with large numbers of resident dendritic cells (DCs). The purpose of this study was to examine the phenotype and distribution of these cells in inflammation. METHODS: Normal and inflamed murine corneas were excised at different time points and immunofluorescence staining with multiple antibodies was performed by confocal microscopy on whole-mounted corneal stromas to characterize and evaluate the distribution of DCs in inflammation. RESULTS: CD11c+CD11b+ myeloid DCs were present throughout the anterior stroma. In the periphery of the normal cornea, nearly one half were major histocompatibility complex (MHC) class II+CD80+CD86+, while they were uniformly MHC class II-CD80-CD86- in the center. In inflammation, in addition to a significant increase in the number of DCs, a majority up-regulated their expression of MHC class II, CD80, and CD86, indicating their state of maturation. The up-regulation of MHC class II and costimulatory molecules on DCs was seen as early as 24 hours after induction of inflammation or transplantation. In addition to the CD11c+DCs in the anterior stroma, a CD11c-CD11b+ population of monocytes/macrophages was present almost exclusively in the posterior stroma of the cornea. These cells were found throughout all layers of the stroma, and in increased numbers, after induction of inflammation. CONCLUSION: The present study demonstrates, for the first time, the phenotypic changes and distribution of resident stromal DCs in corneal inflammation. Clinical Relevance These novel data suggest that the cornea is capable of participating in immune and inflammatory responses by virtue of its own heterogeneous population of DCs.

Animals↗
PubMed1992

Inflammation patterns after laser trabeculoplasty measured with the laser flare meter.

Anterior chamber inflammation was measured in 71 eyes after argon laser trabeculoplasty with the laser flare-cell meter (Kowa FC-1000). Visual acuity, tonometry, and laser flare measurement were performed before and 3, 6, and 18 hours and 2, 4, 7, 14, 30, and 90 days after argon laser trabeculoplasty. Anterior chamber inflammation peaked 2 days after argon laser trabeculoplasty. Forty-nine percent of the eyes showed significant inflammation, with a flare increase of more than 10 photon counts per millisecond over prelaser values. Inflammation was significantly more frequent in pseudoexfoliative glaucoma (69%) and pigmentary glaucoma (100%) than in primary open angle glaucoma (23%). Post-argon laser trabeculoplasty relative pressure decrease was significantly more important in the group of patients with inflammation than in the group without inflammation in the early and late follow-up periods. Topical nonsteroidal anti-inflammatory treatment (diclofenac sodium) was needed in 17 patients, who readily responded to treatment within 72 hours.

Aged↗
PubMed2001

Immune privilege persists in eyes with extreme inflammation induced by intravitreal LPS.

Since immune privilege is believed to exist in the eye in order to suppress sight-destroying inflammation, we wondered whether eyes with intraocular inflammation retain the immune privileged state. Intraocular inflammation was induced by injection of lipopolysaccharide (LPS) into the vitreous cavity of BALB/c mouse eyes, which showed a peak in intensity at approximately 9 h. At this time point, inflamed eyes were examined for their capacity to afford immune privilege to injected allogeneic tumor cells, and to promote anterior chamber-associated immune deviation (ACAID) to antigens injected locally. In addition, aqueous humor (AqH) harvested from inflamed eyes was tested for its ability to suppress T cell activation. Surprisingly, eyes with acute, intense intraocular inflammation allowed allogeneic tumor cells to form progressively growing tumors, and these same eyes promoted ACAID. Moreover, AqH harvested from inflamed eyes strongly inhibited T cell activation. We conclude that the type of extreme, intraocular inflammation evoked by intravitreally injected LPS fails to abolish immune privilege in the eye. These findings are discussed in light of the effects of other types of inflammation on the integrity of ocular immune privilege, and with respect to the capacity of the eye to maintain immune privilege by more than one mechanism.

Animals↗
PubMed1988

Inflammation of rat molar pulp and periodontium causes increased calcitonin gene-related peptide and axonal sprouting.

We have studied the response of nerve fibers containing calcitonin gene-related peptide immunoreactivity (CGRP-IR) to inflammation using a rate dental experimental system. Inflammation was induced by drilling tooth cusps to create pulpal exposures; the induced pulpitis and subsequent periapical lesions were studied 1-35 days later using standard CGRP immunohistochemistry and the avidin-biotin peroxidase method. The injury and resulting inflammation caused a disruption of CGRP-IR nerve fiber location and arborization that varied depending on whether the initial injury was limited to the pulp tip or extended throughout the pulp horn. At shorter survival periods (24 hr, 3 days) nerve fibers were either decreased or bundled into the center of the pulp with sprouting along the wound border. At 6 days necrosis and acute inflammation had advanced to varying degrees, and CGRP-IR fibers were extensively sprouted in the surviving pulp; the pulp also stained specifically for CGRP within 1-2 mm of the inflamed tissue at 6 days. At 35 days, we found total pulp necrosis in most teeth and the development of periapical bone loss, granulomatous tissue, and periapical abscesses. There was also an extensive increase in CGRP-IR nerve fibers in the tissues surrounding sites of severe periodontal inflammation and necrosis. In some cases, macrophage-like cells staining specifically for CGRP were near the abscesses. The results show important interactions between peptidergic nerve fibers and inflammatory cells, and are discussed in terms of the role of nerve fibers containing CGRP in neurogenic inflammation, mechanisms for intensification of CGRP immunoreactivity in affected fibers or neighboring cells, and implications for chronic inflammatory conditions, dental pain, and anesthesia.

Animals↗
PubMed2003

Association between carotid atherosclerosis and markers of inflammation in rheumatoid arthritis patients and healthy subjects.

OBJECTIVE: To examine the relationship between markers of systemic inflammation and carotid atherosclerosis in patients with rheumatoid arthritis (RA) and healthy controls. METHODS: Carotid artery intima-media thickness (IMT) and carotid plaque were measured using high-resolution B-mode ultrasound in 204 patients with RA, ages 40-85, and 102 age- and sex-matched healthy persons. No subject in either group had ever smoked cigarettes. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were used to measure systemic inflammation. The relationship of the carotid artery IMT and carotid plaque to inflammation markers was examined, adjusting for age, sex, RA versus control status, and the cardiovascular (CV) risk factors hypercholesterolemia, systolic blood pressure, diabetes mellitus, and body mass index (BMI). RESULTS: A significant linear trend for increased carotid artery IMT was associated with increasing ESR and CRP categories (r = 0.16, P = 0.004 for ESR, and r = 0.13, P = 0.02 for CRP). These trends did not differ among RA cases and controls, and were independent of age, sex, and CV risk factors. The difference in carotid artery IMT between the lowest and highest categories of ESR was 0.221 mm (95% confidence interval [95% CI] 0.767-1.020, P = 0.02). The difference between extreme CRP categories was 0.275 mm (95% CI 0.039-0.509, P = 0.02). Both remained significant after CV risk factor adjustment. Carotid plaque displayed a similar relationship to markers of inflammation. CONCLUSION: Increased carotid artery IMT and the presence of carotid plaque are associated with markers of systemic inflammation in patients with RA and in healthy subjects. This observation is consistent with hypotheses that assign a role to systemic inflammation in atherosclerosis, and may have implications regarding RA and other chronic inflammatory diseases.

Adult↗
PubMed2003

The pancreatitis-associated protein induces lung inflammation in the rat through activation of TNFalpha expression in hepatocytes.

The pancreatitis-associated protein (PAP) is a pancreatic stress protein overexpressed during acute pancreatitis, a disease often accompanied by lung inflammation. We investigated whether PAP was involved in the occurrence of this remote complication of pancreatitis and whether the liver might be implicated in the process. PAP was injected into the vena cava of rats (40 or 400 micro g/kg body weight). For comparison, pancreatitis was induced in rats by intraductal administration of sodium taurocholate. Three hours later, parameters of inflammation and mRNA concentrations of TNFalpha, P-selectin, heat shock protein (HSP)-70, and extracellular superoxide dismutase (EC-SOD) were monitored in lung and liver. Significant increases in P-selectin expression, neutrophil infiltration, and oxidative stress revealed that PAP treatment induced lung inflammation in rats and exacerbated inflammation in animals with pancreatitis. Plasma TNFalpha level was increased and TNFalpha mRNA was strongly overexpressed in liver, with concomitant activation of NF-kappaB; in situ hybridization revealed that TNFalpha overexpression was mainly located to hepatocytes. Lung inflammation induced by PAP could be prevented by injection of anti-TNFalpha antibodies. It was concluded that, during pancreatitis, PAP released by the pancreas could mediate lung inflammation through induction of hepatic TNFalpha expression and subsequent increase in circulating TNFalpha.

Animals↗
PubMed2002

Protective effect of prior acute immune challenge, but not footshock, on inflammation in the rat.

Previous studies have revealed that a single exposure to an acute stress or acute immune stimulus can produce long-lasting changes in the activity and responsiveness of the hypothalamo-pituitary-adrenal (HPA) axis. The HPA axis is believed to be an important component in determining the susceptibility and severity of inflammation in autoimmune disease models such as adjuvant-induced arthritis (AA). In the present study we have tested the hypothesis that a single exposure to either footshock or lipopolysaccharide (LPS) 3 weeks prior to adjuvant injection can alter susceptibility to AA. Changes in HPA axis parameters were also determined. The results demonstrated that prior exposure to LPS conferred resistance to inflammation in AA, which was not related to a delay in onset of inflammation but rather an alteration in susceptibility. In contrast, prior exposure to the acute stress of footshock did not alter susceptibility. HPA axis parameters were increased in adjuvant-injected rats whether inflammation was present or not. These data suggest that prior exposure to acute immune stimuli, but not to acute footshock stress, may alter susceptibility to inflammation in the rat AA model. These changes in susceptibility do not appear to be solely mediated by increases in HPA axis activity, which were apparent in all AA groups irrespective of the presence of inflammation.

Acute Disease↗
PubMed1999

Impact of gender on exocrine gland inflammation in mouse models of Sjögren's syndrome.

Sjögren's syndrome is a complex autoimmune disorder, that occurs almost exclusively in females, induces extensive lymphocyte accumulation in lacrimal and salivary glands, and represents one of the leading causes of dry eye and mouth in the world. The purpose of this study was to determine whether the profound, gender-related differences observed in the magnitude of exocrine gland inflammation in Sjögren's syndrome may also be found in tissues of mouse models of this disorder. Lacrimal and submandibular glands were obtained from adult MRL/lpr, MRL+/+ (MRL+), NZB/NZW F1 (F1), C3H/lpr, C3H/gld (gld), C57BL/6-lpr/lpr [B6/lpr; with (bcl-2(+)/lpr) or without (bcl-2(-)/lpr) bcl-2 transgene insertion] and nonobese diabetic (NOD) mice after the onset of autoimmune disease, and processed for microscopy and image analysis. Our results showed that: (1) the extent of inflammation was significantly greater in lacrimal glands of female MRL/lpr, MRL+, F1, C3H/lpr and gld mice, and salivary glands of female MRL+, F1 and gld mice, relative to those of males; (2) the severity of inflammation in NOD mice showed a tissue-specific pattern: inflammation was far worse in lacrimal glands of males, whereas immune pathology was far greater in salivary tissues in females; and (3) no gender-related variations were present in the degree of inflammation in lacrimal glands of bcl-2(+)/lpr and bcl-2(-)/lpr mice or in submandibular tissues of MRL/lpr, C3H/lpr, bcl-2(+)/lpr and bcl-2(-)/lpr mice. Our findings demonstrate that gender-, strain- and tissue-related differences exist in the extent of inflammation in several mouse models of Sjögren's syndrome.

Animals↗