No abstract

As a cytoplasmic protein tyrosine kinase, Bruton's tyrosine kinase (Btk) is widely considered as a vital kinase in many aspects of different physiologic processes. It is engaged in many important signalling pathways related to the immune response, such as the B cell receptor pathway, pattern‐recognition receptor pathway, and triggering receptor expressed on myeloid cell pathway. Recent studies have increasingly focused on the important role of Btk in various inflammatory diseases, which are related to Btk expression in myeloid innate immune cells, such as macrophages, dendritic cells and neutrophils. Although some investigations have explored the role of Btk in microbial infections, many aspects remain elusive, and some of the results are opposite and controversial. Considering the complicated and multiple roles of Btk in the immune system, we summarized the engagement of Btk signalling in various pathogenic microorganism infections, the possible mechanisms involved and its therapeutic potential in the control of infectious diseases.

Acetaminophen (APAP) is a kind of widely used drug for the treatment of pain and fever. It is reported that its overdose can cause serious liver failure. 1 In Europe and the United States, APAP-induced acute liver injury (ALI) has become one of the primary causes of liver failure and thus arises widespread concern and research in the world. 2 Abundant evidences have suggested that both innate and adaptive immune cells, such as macrophages, neutrophils and T cells, played critical roles in APAP-induced ALI. 3,4 It is now clear that neutrophils have important homeostatic functions in various organ systems including liver, 5,6 but what the role of neutrophils plays in APAP-induced ALI still remains elusive. 7,8 Neutrophils, a type of polymorphonuclear leukocytes, are the first-line guardians of the innate immune system. Normally, neutrophils are not activated and move slowly in peripheral blood circulation without direction. The half-life of neutrophils is only 6-7 hours. 9 Once the pathogen invades or the endogenous stimulants releases, the pattern recognition receptors can recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Then, inflammatory reaction occurs and neutrophils are activated. 10,11 The activated neutrophils in peripheral circulation will tend to move towards the injury site. The migration of neutrophils involves rolling, activation and adhesion. 12,13 They then participate in the inflammatory process through phagocytosis, degranulation and extracellular traps (NETs). 14 On the one hand, neutrophils are drawn from the blood to sterility inflammatory site, which contribute to wound healing. On the other hand, their prolonged half-life, release of granule proteins such as myeloperoxidase (MPO), neutrophil serine proteases (NSPs), lipocalin 2 (LCN2), human neutrophil peptide (HNP), excessive infiltration and uncontrolled activation may lead to destruction of normal tissue structures and serious inflammations. 15 Therefore, how neutrophils play in APAP-induced ALI has aroused great controversy. In this review, we outline the neutrophil's

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