Role of Bacteria in Dermatological Infections
K. Balamurugan, U. Prithika in Pocket Guide to Bacterial Infections, 2019
S. epidermidis is a ubiquitous gram-positive skin and mucosal membrane colonizer, which exerts a mutualistic relationship with host. It forms the major part of microbial barrier that precludes the colonization of other pathogens. In a competitive environment, it secretes lantibiotics (i.e., lanthionine-containing antibacterial peptides) often referred as bacteriocins, which prevent the colonization of S. aureus and GAS (Sahl, 1994; Cogen et al., 2007). Also, accessory gene regulator (agr) locus found in commensal S. epidermidis produces peptide pheromones that activate the agr QS system of competing bacteria, which in turn, reduces colonization and down-regulates the expression of virulence factors by increasing the production of pheromones such as phenol soluble modulin (Otto, 2001). In addition, S. epidermidis boosts the host immune defense by eliciting the signaling of toll like receptor (TLR). The pattern recognition receptors TLRs, in turn, specifically recognize different pathogen-associated molecular patterns and activate the host immune system accordingly.
Host Defense and Parasite Evasion
Eric S. Loker, Bruce V. Hofkin in Parasitology, 2023
When infected with a protozoan, a host’s innate immune system must rapidly detect and respond to the parasite. Failure to do so allows the parasite to overwhelm the host, with disease and possibly death as likely outcomes. In this way, the response to protozoa is no different from the response to other microparasites. For many years it was unclear how the initial detection was achieved. In the past few decades it has become apparent that various immune system cells bear pattern recognition receptors (PRRs) that recognize certain molecules associated with specific groups of pathogens (PAMPs). As previously described in terms of their function in the plant immunoresponse, PAMPs essentially act as “danger signals”, alerting the immune system that a certain type of infection has occurred.
Defence Mechanisms
John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie in Basic Sciences Endocrine Surgery Rhinology, 2018
The immediate response to an invading pathogen is mounted by innate components resident within the infected tissues (Figure 13.1a). In particular, tissue macrophages (and other cells with innate immune functions) express a range of pattern recognition receptors for microbial structures, including mannose receptor, scavenger receptors and Toll-like receptors, whose ligands include various microbial polysaccharides, lipids and nucleic acids. Complement proteins are also directly activated by microbes via the alternative pathway (see ‘The Complement System’ below). Inflammatory products of macrophages and complement, together with those released by tissue mast cells activated by the complement peptides C3a and C5a (known as anaphylatoxins), induce the migration of granulocytes, natural killer cells and more complement proteins from the blood stream into the infected tissues (Figure 13.1b).
Cytokine production and outcome in MDR versus non-MDR gram-negative bacteraemia and sepsis
Published in Infectious Diseases, 2021
Vasileios Karamouzos, Evangelos J. Giamarellos-Bourboulis, Dimitrios Velissaris, Theologia Gkavogianni, Charalambos Gogos
The first line of defence following pathogen invasion is the innate immune system. Special pattern recognition receptors (PRRs) that are expressed in a variety of cells initiate the hosts immune response by detecting pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). PRR activation initiates the release of pro-inflammatory cytokines, resulting in leukocyte recruitment and activation of the coagulation and complement systems [10]. Previous studies in animal models have demonstrated immune response and virulence differences between isolates with distinct susceptibility patterns. Giamarellos-Bourboulis et al. showed that infection by susceptible P. aeruginosa in rabbits was accompanied by higher TNF-α levels and reduced survival when compared to animals inoculated with MDR strains [11]. Zhou et al. using three different isolates of K. Pneumoniae found that pan-drug resistant isolates are causing less damage compared to MDR and susceptible isolates [12]. In our study, levels of the potent pro-inflammatory cytokine TNF-α, were significantly lower in patients with sepsis caused by resistant pathogens suggesting that the induced immune response may differ depending on the susceptibility patterns of the pathogens. While there was a significant difference in TNF-α levels between MDR and non-MDR this pattern was not observed with the rest cytokines measured.
Role of platelets and megakaryocytes in adaptive immunity
Published in Platelets, 2021
Genevieve Marcoux, Audrée Laroche, Jenifer Espinoza Romero, Eric Boilard
The ability of an organism to defend itself against foreign substances and infectious agents principally requires contributions from two components of the immune system, namely innate or natural immunity and acquired, also known as adaptive, immunity. The innate immune response implicates the recognition of well-conserved molecular motifs, known as pathogen-associated or damage-associated molecular patterns (respectively PAMPs or DAMPs). Pathogen-associated molecular patterns are exogenous components conserved among a large spectrum of microorganisms and allergens, while DAMPs, derived from host cells, are endogenous alarm signals produced during cellular stress or death and lead to sterile inflammatory responses [1,2]. PAMPs and DAMPs bind to cell surface receptors and intracellular sensors known as pattern recognition receptors (PRRs), which include the Toll-like receptors (TLRs), NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), and C-type lectin-like receptors (CLRs). Pattern recognition receptors are expressed by innate immune cells and nonimmune cells. Innate immune responses are nonspecific and do not confer long-lasting immunity.
Repurposing of the childhood vaccines: could we train the immune system against the SARS-CoV-2
Published in Expert Review of Vaccines, 2021
Heterologous protective effects of vaccines are usually governed by innate immune cells (natural killer cells and monocytes) that show the memory-like response and are popularly called trained immunity [24,25]. Trained immunity occurs due to epigenetic reprogramming through histone modifications that further transform the expression patterns of several genes and have shown the protective effects against secondary infections [29]. Increased intensity of the pattern recognition receptors on the surface of innate immune cells may involve the recognition of pathogens and further their clearance through inflammatory responses [30]. Earlier research also showed that autophagy, a phenomenon of the proteolytic degradation of cytosolic components at the lysosome, contributed to BCG-induced trained immunity [31]. Cross-reactivity is another means which can contribute to heterologous protective effects of vaccines because these vaccines possess similar cross-reactive antigenic epitopes from the original antigens as well as antigens of other infectious diseases [28].
Related Knowledge Centers
- Adaptive Immune System
- Innate Immune System
- Lipopolysaccharide
- Lipoteichoic Acid
- Mannose
- Peptidoglycan
- Protein
- Pathogen
- Pathogen-Associated Molecular Pattern
- Damage-Associated Molecular Pattern