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Chlamydiae are Gram-negative bacteria, which replicate exclusively in the infected host cells. Infection of the host cells by Chlamydiae stimulates the innate immune system leading to an inflammatory response, which is manifested not only by secretion of proinflammatory cytokines such as IL-1 β  from monocytes, macrophages, and dendritic cells, but also possibly by cell death mediated by Caspase-1 pyroptosis. RIP3 is a molecular switch that determines the development of necrosis or inflammation. However, the involvement of RIP3 in inflammasome activation by  Chlamydia muridarum  infection has not been clarified. Here, we assessed the role of RIP3 in synergy with Caspase-1 in the induction of IL-1 β  production in BMDM after either LPS/ATP or  Chlamydia muridarum  stimulation. The possibility of pyroptosis and necroptosis interplays and the role of RIP3 in IL-1 β  production during  Chlamydia muridarum  infection in BMDM was investigated as well. The data indicated that RIP3 is involved in NLRP3 inflammasome activation in LPS/ATP-stimulated BMDMs but not in  Chlamydia muridarum  infection. Pyroptosis occurred in BMDM after LPS/ATP stimulation or  Chlamydia muridarum  infection. Moreover, the results also illuminated the important role of the Caspase-1-mediated pyroptosis process which does not involve RIP3. Taken together, these observations may help shed new light on details in inflammatory signaling pathways activated by  Chlamydia muridarum  infection.

biomed research international

<i>Chlamydia muridarum</i>Infection of Macrophages Stimulates IL-1<i>β</i>Secretion and Cell Death via Activation of Caspase-1 in an RIP3-Independent Manner

Chlamydia muridarumInfection of Macrophages Stimulates IL-1βSecretion and Cell Death via Activation of Caspase-1 in an RIP3-Independent Manner