Formation of Autoimmune Lesions Is Independent of Antibiotic Treatment in NOD Mice

Abstract

The relationship between autoimmunity and changes in intestinal microbiota is not yet fully understood. In this study, the role of intestinal microbiota in the onset and progression of autoimmune lesions in non-obese diabetic (NOD) mice was evaluated by administering antibiotics to alter their intestinal microenvironment. Flow cytometric analysis of spleen cells showed that antibiotic administration did not change the proportion or number of T and B cells in NOD mice, and pathological analysis demonstrated that autoimmune lesions in the salivary glands and in the pancreas were also not affected by antibiotic administration. These results suggest that the onset and progression of autoimmunity may be independent of enteral microbiota changes. Our findings may be useful for determining the appropriate use of antibiotics in patients with autoimmune diseases who are prescribed drugs to maintain systemic immune function.

Profiling the Gut Microbiome Unraveled Signature Bacterial Groups in Autoimmune Diabetes, which Remain Unperturbed by the Low Ionic Strength of the Drinking Water in NOD mice

“…However, commensal bacteria have been implicated in modulating autoimmune responses against insulin-producing β cells and, hence, diabetes [20][21][22]. Broad-spectrum antibiotics mostly worsened diabetes [23,24,[36][37][38], except for the marginal protection reported in one study [24]. Interestingly, a mixture of broad-spectrum antibiotics, ampicillin, metronidazole, and neomycin administered to adult NOD mice failed to inhibit diabetes development despite decreasing the gut microbiome [38].…”

“…Broad-spectrum antibiotics mostly worsened diabetes [23,24,[36][37][38], except for the marginal protection reported in one study [24]. Interestingly, a mixture of broad-spectrum antibiotics, ampicillin, metronidazole, and neomycin administered to adult NOD mice failed to inhibit diabetes development despite decreasing the gut microbiome [38]. Providing probiotics also yielded mixed results on protection against diabetes [39][40][41][42][43][44].…”

A Glimpse Into the Microbiome of Sjögren’s Syndrome

“…Along with these reports that questioned the role autoimmunity plays in the microbiota dysbiosis of SS, one possible reason to explain the microbiota changes is that the alteration of the microbiome is the leading factor of clinical symptoms as well as the breakdown of autoimmune system. After all, other studies also reported that microbial dysbiosis can occur independent of salivary deficiency and SS can be developed independent of microbiome changes (18,30).…”

The proportion of CD161 on CD56+NK cells in peripheral circulation associates with clinical features and disease activity of primary Sjögren’s syndrome

“…Primary Sjogren's syndrome(pSS) is a complex autoimmune disease, which is characterized by the infiltration of lymphocytes from exocrine glands, leading to the dysfunction of gland secretion, and then a series of symptoms of gland injuries, such as dry mouth, dry eye and swelling of parotid gland, as well as extraglandular manifestations such as arthralgia, interstitial lung disease(ILD), renal tubular acidosis and primary biliary cholangitis(PBC),and part of patients have systemic manifestations, such as fatigue, fever and weight loss [1,2] . Until now, the pathogenesis of pSS has not been clarified.Generally speaking, the pathogenesis of pSS is related to environmental factors,genetic susceptibility and immune disorder.It is well known that pSS is mainly mediated by T cells and B cells, but innate immune cells such as NK cells also play an important role in the pathogenesis of pSS [3] .Recent studies have found that the expression of NK cells in peripheral blood or salivary glands of pSS patients or model mice was abnormal, which was related to the activity and severity of the disease [4][5][6] .…”