Bacterial Recognition and Induced Cell Activation in Sepsis

Abstract

The pathogenesis of sepsis involves complex interaction between the host and the infecting microorganism. Recognition and processing of microorganism antigens are essential functions of the cells of innate immune systems, and will ultimately, through the antigen presentation to the cells of adaptive immunity and the synthesis and secretions of mediators, such as cytokines, drive a coordinated immune response. Neutrophils and monocytes will therefore function as sensing and effectors cells. Fundamental in this process is the ability to discriminate self from non-self molecules. Of major interest in sepsis is that the protective and damaging host responses are part of the same process, that is, the inflammatory response that controls the infection process also underscores many of the pathophysiological events of sepsis. Moreover, this is a dynamic process according to the continuum of sepsis and its complications; up and down regulation of cellular activities may be differently regulated in different tissues, different cells and even in different functions of the same cell. This review will focus on microorganism recognition and signalization in sepsis, with emphasis on the neutrophils and monocytes adaptation during the ongoing disease.

Association of mannose-binding lectin-2 genotype and serum levels with prognosis of sepsis

“…The importance of the interactions between pathogen-associated microbial patterns and mannose-binding lectin (MBL) in activating innate immunity has been considered as a component of the innate immune system [9]. Moreover, it is now recognized that the first response to invasion (i.e., innate immunity) has a significant influence on the subsequent adaptive response [10,11]. …”

Sepsis and Acute Kidney Injury

“…15,16 After initial host-microbial interactions, there is widespread activation of the innate immune response, which coordinates a defensive response involving both humoral and cellular components. 17 This in turn leads to secretion of various cytokines, most importantly IL-1, 18 TNF-␣, 19 and IL-6, 20 that progress to a state of cytokine storm, hemodynamic instability, and eventually organ dysfunction and septic shock. The precise nature of such hemodynamic instability and its consequence on renal blood flow (RBF) will be discussed in more detail below.…”

The role of peroxisome proliferator-activated receptors in the pathogenesis of insulin resistance and septic shock

“…Enflamasyonun başlaması ile birlikte sitokinler, adezyon molekülleri, reaktif oksijen ve nitrojen türleri gibi mediyatörlerin aşırı ve kontrolsüz bir biçimde oluşumunun artması sepsis patofizyolojisine katkıda bulunmaktadır. Sepsiste oluşum-ları artan TNF-α, IL-1, IL-8 ve interferon (interferon; IFN)-γ gibi enflamasyonun başlamasına aracılık eden sitokinlerin yanı sıra, IL-4, IL-10 ve IL-13 gibi antienflamatuvar sitokinler de oluşmaktadır (49,(51)(52)(53)(54)(55)(56)(57)(58)(59)(60)(61)(62)(63).…”