Opportunistic Intracellular Bacteria and Immunity (Infectious Agents and Pathogenesis)

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These can range from common skin and mucosal infections, to a serious life-threatening sepsis and organ failure. In both cases, there are few treatments available, and there are no available vaccines. Table 1. Common fungal pathogens and some of the infections they cause, usually in immunocompromised patients. TLR2 Figure 1. CARD9 is the most important molecule for activating antifungal immune responses discovered to date. Register Log in.

Immune responses to fungal pathogens Download Immune responses to fungal pathogens.

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Opportunistic Intracellular Bacteria and Immunity (Infectious Agents and Pathogenesis) [Lois J. Paradise, Herman Friedman, Mauro Bendinelli] on jerowerdori.ml Opportunistic Intracellular Bacteria and Immunity. Infectious Agents and Pathogenesis Immune Defenses against Intracellular Bacterial Infections. Pages

Rebecca A. Drummond, University of Birmingham, UK.

Opportunistic infection

Fungal Species Types of Infection Candida albicans Vulvovaginal candidiasis thrush Oral candidiaisis mouth infection Disseminated candidiasis sepsis Aspergillus fumingatus Invasive pulmonary aspergillosis lung infection Pneumocystis carinii Pneumonia lung infection Cryptococcus neoformans Cryptococcosis lung infections, meningitis Table 1.

Figure 1. A dendritic cell decorated with anti-fungal PRRs. Related Articles Candida albicans. Chlamydia Trachomatis.

Autoimmunity Can Predispose to Infectious Diseases

Aspergillus fumigatus. Candida albicans. In addition, IL deficient mice have been shown to be susceptible to various pyogenic infections, including Streptococcus pneumoniae , Pseudomonas aeruginosa , and Klebsiella pneumoniae [23] — [26]. Interestingly, autoantibodies to IL-6 were not identified in other patients with severe staphylococcal diseases and hence suggest that anti-IL-6 autoantibodies were not generated due to molecular mimicry with Staphylococcus aureus.

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In addition, the course of clinical events in the patient was suggestive of an occurrence of anti-IL-6 autoantibodies that preceded staphylococcal infection. GM-CSF has a key role in enhancing the antimicrobial activities of neutrophils and macrophages by augmenting the expression of CD11b, an adhesion molecule that mediates neutrophil adhesion to endothelial cells, and hence promoting the recruitment of neutrophils to the site of infection; promoting the differentiation of macrophages and dendritic cells DCs ; and by priming the phagocytosis and bactericidal activities of these cells.

In addition, these autoantibodies exist abundantly in the lungs, and by effectively blocking GM-CSF binding to its receptor, they specifically inhibit alveolar macrophage differentiation, phagocytosis, and surfactant catabolism [30] , [31]. Th17 cytokines are implicated in protection against fungal infections, including Candida at mucosal surfaces, and hence neutralizing antibodies to Th17 cytokines can predispose to fungal infections [8] , [34] , [35].

Of particular importance, the autoantibody titers were high before the onset of CMC.

Taken together, anti-cytokine autoantibodies induce an acquired immune-compromised state that predisposes the host to infections. Although autoantibodies to several cytokines are relatively widespread, they rarely neutralize to a significant extent [39]. Further, anti-cytokine autoantibodies do not seem to have co-distribution, and cytokines do have redundant functions; hence, severe infections are not common unless as described above, and neutralizing autoantibodies are developed against specific cytokines that are key in an anti-microbial response.

In view of these findings, we suggest that patients with uncontrolled or repeated infections despite antimicrobial therapy should be considered for screening and evaluating autoimmunity. Although reported examples are of autoantibodies to cytokines, the occurrence of autoantibodies that target either molecules implicated in the recognition of pathogens such as Toll-like receptors and lectin receptors or antigen presenting and co-stimulatory molecules cannot be ruled out.

Indeed, genetic defects or polymorphisms in pattern recognition receptors and their signaling pathways and susceptibility to infections have been reported [41] — [44].

Introduction

View Article Google Scholar 6. T cell-derived IL antagonizes macrophage function in mycobacterial infection. During periodontal infection the quantities of periodontal pathogens increases dramatically leading to transient bacteraemia [ 84 — 86 ]. You can write a opinion file and reload your people. We ca however use to impact the download the biology of genetic dominance you facilitate trying for.

Despite the reports of anti-cytokine antibodies in several malignant or infectious diseases and their low titers in healthy individuals, the high titers are predominant in autoimmune diseases [39]. Here, AIRE autoimmune regulator , a novel gene that regulates peripheral self-antigen expression in medullary thymic epithelia and DCs, is mutated, leading to disturbed self-tolerance mechanisms.

Further, extensive work by the Meager and Willcox group provided clues toward autoimmunizing mechanisms and innate cells plasmacytoid and myeloid DCs in the induction of anti-cytokine antibodies to type I IFNs and IL [39] , [40] , [45]. Therefore, it is probable that autoantibodies are produced as a consequence of infections and these autoantibodies subsequently exacerbate the infectious diseases or, alternatively, a cryptic autoimmunity develops due to unknown reasons that predispose the individual to infections.

Infectious agents and vaccines are often thought to be one of the environmental factors that induce autoimmunity either by molecular mimicry, epitope spreading, bystander activation of immune system, or polyclonal activation of immune cells [2] , [3].

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It is thus likely that in case of chronic persistent diseases such as tuberculosis, a pathogen might trigger the autoimmune process by one of these mechanisms. Indeed, the majority of patients with autoantibodies and mycobacterial infections originated from disease-endemic areas [13] — [20].

Therefore, dissection of underlying causes of autoimmunity such as genetic polymorphisms, gene deficiency, or environmental factors might shed light on these unanswered questions. Therapeutic strategies for autoimmunity-associated infectious diseases should be aimed at controlling the infection as well as inhibiting the autoimmune response: blocking autoantibody-producing B cells and neutralizing autoantibodies. In this context, a combination of anti-microbial agents and immunosuppressive treatments represents a classical line of therapy for autoimmunity-associated infectious diseases.

Plasmapheresis that removes autoantibodies or supplementing exogenous cytokines against which autoantibodies have developed are other potential therapeutic strategies. However, such therapeutic strategies do not eliminate the source of autoantibodies, i.

However, repeated cycles of B cell—targeted therapies can lead to a reduction in total immunoglobulin level and predisposition to serious infections [49] , [50]. Also, these therapeutic agents do not target antibody-producing plasma cells. In view of proven safety and efficacy in diverse autoimmune diseases, polyclonal intravenous immunoglobulin IVIg in combination with anti-microbial agents represents an attractive therapy for autoimmunity-associated infections [51].

Since IVIg is obtained from pooled plasma of several thousand healthy blood donors, based on the exposure of donors to infectious diseases and vaccinations, IVIg contains antibodies to a wide range of infectious agents, and hence these anti-microbial antibodies within IVIg preparations can directly neutralize pathogens [53]. However, determining an effective dose regimen and duration of IVIg therapy needs further investigation. Indeed, the combination of B cell—targeted therapies and IVIg has been successfully used in several autoimmune and inflammatory diseases [54] , [55]. Autoimmunity Can Predispose to Infectious Diseases During the course of autoimmunity, autoantibodies that can neutralize key components of the immune system that are essential in mounting anti-microbial responses may be produced Figure 1.

Download: PPT. Figure 1. Host immune response to pathogens and predisposition to infections due to autoimmunity. Specific Examples of Autoimmunity Favoring Infectious Diseases Several reports have now demonstrated the occurrence of neutralizing autoantibodies against cytokines in patients with infections. Enigma of Induction of Anti-Cytokine Autoantibodies Despite the reports of anti-cytokine antibodies in several malignant or infectious diseases and their low titers in healthy individuals, the high titers are predominant in autoimmune diseases [39].

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Therapeutic Options for Autoimmunity-Associated Infectious Diseases Therapeutic strategies for autoimmunity-associated infectious diseases should be aimed at controlling the infection as well as inhibiting the autoimmune response: blocking autoantibody-producing B cells and neutralizing autoantibodies. References 1. Shoenfeld Y Idiotypic induction of autoimmunity: a new aspect of the idiotypic network. View Article Google Scholar 2. Trends Immunol — View Article Google Scholar 3. Nat Rev Rheumatol 5: — View Article Google Scholar 4. J Autoimmun — View Article Google Scholar 5.

Hewagama A, Richardson B The genetics and epigenetics of autoimmune diseases. J Autoimmun 3— View Article Google Scholar 6. Blood — View Article Google Scholar 7. Nature — View Article Google Scholar 8.