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TLRs and NLRs participate in the immune system recognition of Helicobacter pylori. However, little is known about the mechanisms leading to inflammasome activation by H. pyloriand if NLRs in neutrophils are involved in the process. We studied how NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome components are involved in IL-1β maturation in human neutrophils in response to the infection and if they are dependent on T4SS (type IV secretion system) and TLRs. Human neutrophils were cultured and infected with the 26695 or the VirD4−H. pyloristrains; the IL-1β concentration was analyzed by ELISA, and we also evaluated the activation of TLRs 2 and 4. The infection of neutrophils with both strains of H. pyloriinduced production of IL-1β and expression of the NLRP3 inflammasome components such as apoptosis-associated speck-like protein with CARD domain and NLRP3 protein. The infection also increased the activity of caspase-1, which is required for the maturation of IL-1β. Our study shows, for the first time, that H. pyloriinfection induces the expression and activation of components of NLRP3 inflammasomes in human neutrophils and that the activation is independent of a functional T4SS and TLR2 and TLR4.

Colonization of the gastric mucosa by Helicobacter pylorican lead to peptic ulcer and gastric adenocarcinoma. TLRs are signaling receptors involved in the recognition of microorganisms, and polymorphisms in their genes may influence the innate and adaptive immune response to H. pylori, affecting the clinical outcomes of the infection. We assessed the association between single nucleotide polymorphisms in TLR9and TLR5and gastroduodenal diseases. All patients were genotyped by allelic discrimination in regions 1174C > T and 1775A > G of TLR5and −1237T > C and 2848G > A of TLR9. The 2848A allele of TLR9was more frequent in duodenal ulcer and showed an association of risk with this pathology. Polymorphisms in TLR5were not found to be associated with disease. Patients with polymorphisms in TLR9and TLR5expressed significantly lower levels of IL-1β and TNF-α, whereas polymorphisms in TLR5also decreased the expression of IL-6 and IL-10. Our findings suggest that 2848G > A polymorphism in TLR9increases the risk for the development of duodenal ulcer probably by modifying the inflammatory response to H. pyloriinfection. This is the first study to show an association of 2848A allele of TLR9with duodenal ulcer and with altered expression of inflammatory cytokines in the gastric mucosa.

At the end of 2019, an outbreak of a severe respiratory disease occurred in Wuhan China, and an increase in cases of unknown pneumonia was alerted. In January 2020, a new coronavirus named SARS-CoV-2 was identified as the cause. The virus spreads primarily through the respiratory tract, and lymphopenia and cytokine storms have been observed in severely ill patients. This suggests the existence of an immune dysregulation as an accompanying event during a serious illness caused by this virus. Natural killer (NK) cells are innate immune responders, critical for virus shedding and immunomodulation. Despite its importance in viral infections, the contribution of NK cells in the fight against SARS-CoV-2 has yet to be deciphered. Different studies in patients with COVID-19 suggest a significant reduction in the number and function of NK cells due to their exhaustion. In this review, we summarize the current understanding of how NK cells respond to SARS-CoV-2 infection.