Inflammasome and Microbiota Functions in Skin, Mouth, and Gut Inflammation

Dear Colleagues,

The intracellular receptors, such as NLRP1, NLRP3, NAIP-NLRC4 (NLR family), AIM2 (ALR family), and Pyrin (TRIM family) are the major proteins known to form inflammasome upon activation. Inflammasome is a multimeric protein complex for activation of caspase-1 and subsequent cleavage of pro-forms of IL-1β and IL-18 to mature forms. Inflammasome formation is crucial in the immunological responses against pathogens. The role of inflammasome in the maintenance of commensal microbiota and related homeostasis is evident through several studies, especially in gastro-intestinal tract homeostasis. Oral mucosal microbiota, dysbiosis, and immune responses are relevant in the inflammatory bowel disease pathogenesis. The function of gastric microbiota in the case of Helicobacter pylori infection and associated diseases must also be addressed. Generally, various microbiota functions are closely associated with the host immune responses, including inflammasome activation.

Several genetic mutations and polymorphisms of inflammasome components are associated with skin inflammation. The skin harbors many microbiota members to regulate immune responses and maintain cutaneous homeostasis. The role of skin microbiota in a wound is correlated with the healing process. Various skin diseases, such as atopic dermatitis, psoriasis, rosacea, acne vulgaris, and even skin cancer, have links with dysbiosis. In addition, the involvement of skin–gut axis microbiota in the etiology of skin diseases is another major aspect to be considered in this scenario.

In the above context, we invite researchers to contribute with original research articles and reviews. It will elaborate functions of microbiota, dysbiosis, and inflammation in the diseases and homeostasis of interconnected epidermal and mucosal surfaces. Therefore, researchers are encouraged to submit their articles in this Special Issue.

Dr. Suneesh Kumar Pachathundikandi
Dr. Gopalakrishnan Sandeep
Guest Editors

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