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1.
FEMS Microbiol Rev ; 38(6): 1146-71, 2014 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-25065463

RESUMO

The complement and coagulation systems are two related protein cascades in plasma that serve important roles in host defense and hemostasis, respectively. Complement activation on bacteria supports cellular immune responses and leads to direct killing of bacteria via assembly of the Membrane Attack Complex (MAC). Recent studies have indicated that the coagulation system also contributes to mammalian innate defense since coagulation factors can entrap bacteria inside clots and generate small antibacterial peptides. In this review, we will provide detailed insights into the molecular interplay between these protein cascades and bacteria. We take a closer look at how these pathways are activated on bacterial surfaces and discuss the mechanisms by which they directly cause stress to bacterial cells. The poorly understood mechanism for bacterial killing by the MAC will be reevaluated in light of recent structural insights. Finally, we highlight the strategies used by pathogenic bacteria to modulate these protein networks. Overall, these insights will contribute to a better understanding of the host defense roles of complement and coagulation against bacteria.


Assuntos
Fenômenos Fisiológicos Bacterianos , Coagulação Sanguínea/imunologia , Proteínas do Sistema Complemento/imunologia , Estresse Fisiológico , Bactérias/imunologia , Infecções Bacterianas/imunologia , Infecções Bacterianas/microbiologia , Interações Hospedeiro-Patógeno/imunologia
2.
Immunity ; 40(2): 213-24, 2014 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-24508233

RESUMO

T cell effector functions can be elicited by noncognate stimuli, but the mechanism and contribution of this pathway to the resolution of intracellular macrophage infections have not been defined. Here, we show that CD4(+) T helper 1 (Th1) cells could be rapidly stimulated by microbe-associated molecular patterns during active infection with Salmonella or Chlamydia. Further, maximal stimulation of Th1 cells by lipopolysaccharide (LPS) did not require T-cell-intrinsic expression of toll-like receptor 4 (TLR4), interleukin-1 receptor (IL-1R), or interferon-γ receptor (IFN-γR) but instead required IL-18R, IL-33R, and adaptor protein MyD88. Innate stimulation of Th1 cells also required host expression of TLR4 and inflammasome components that together increased serum concentrations of IL-18. Finally, the elimination of noncognate Th1 cell stimulation hindered the resolution of primary Salmonella infection. Thus, the in vivo bactericidal capacity of Th1 cells is regulated by the response to noncognate stimuli elicited by multiple innate immune receptors.


Assuntos
Imunidade Inata/imunologia , Inflamassomos/metabolismo , Transdução de Sinais , Células Th1/imunologia , Receptores Toll-Like/metabolismo , Animais , Carga Bacteriana/imunologia , Antígenos CD4/imunologia , Chlamydia/fisiologia , Citometria de Fluxo , Interleucina-18/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Reação em Cadeia da Polimerase em Tempo Real , Salmonella/fisiologia , Receptor 4 Toll-Like/metabolismo
3.
Nature ; 496(7444): 233-7, 2013 Apr 11.
Artigo em Inglês | MEDLINE | ID: mdl-23542589

RESUMO

Our innate immune system distinguishes microbes from self by detecting conserved pathogen-associated molecular patterns. However, these are produced by all microbes, regardless of their pathogenic potential. To distinguish virulent microbes from those with lower disease-causing potential the innate immune system detects conserved pathogen-induced processes, such as the presence of microbial products in the host cytosol, by mechanisms that are not fully resolved. Here we show that NOD1 senses cytosolic microbial products by monitoring the activation state of small Rho GTPases. Activation of RAC1 and CDC42 by bacterial delivery or ectopic expression of SopE, a virulence factor of the enteric pathogen Salmonella, triggered the NOD1 signalling pathway, with consequent RIP2 (also known as RIPK2)-mediated induction of NF-κB-dependent inflammatory responses. Similarly, activation of the NOD1 signalling pathway by peptidoglycan required RAC1 activity. Furthermore, constitutively active forms of RAC1, CDC42 and RHOA activated the NOD1 signalling pathway. Our data identify the activation of small Rho GTPases as a pathogen-induced process sensed through the NOD1 signalling pathway.


Assuntos
Proteína Adaptadora de Sinalização NOD1/metabolismo , Salmonella typhimurium/metabolismo , Salmonella typhimurium/patogenicidade , Proteínas rho de Ligação ao GTP/metabolismo , Animais , Proteínas de Bactérias/metabolismo , Citosol/metabolismo , Feminino , Células HEK293 , Proteínas de Choque Térmico HSP90/metabolismo , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , NF-kappa B/metabolismo , Proteína Adaptadora de Sinalização NOD2/metabolismo , Peptidoglicano/metabolismo , Proteína Serina-Treonina Quinase 2 de Interação com Receptor/metabolismo , Salmonella typhimurium/genética , Transdução de Sinais , Fatores de Virulência/metabolismo , Proteína cdc42 de Ligação ao GTP/metabolismo , Proteínas rac1 de Ligação ao GTP/metabolismo , Proteína rhoA de Ligação ao GTP/metabolismo
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