PubMed Health⌕ Search

PubMed · 8641520

Host factors affecting disease transmission.

Abstract

In prevention of transmission of infectious disease, the host uses a variety of protective mechanisms and can elicit many different responses. Nonspecific defense mechanisms include an intact integument (skin and mucous membranes). The host also can use specialized substances it may secrete, such as mucin or fatty acids to prevent colonization or to inhibit growth of potential pathogens. Specialized surface structures are also used by the host in prevention of disease transmission. These structures include cells composed of keratin and cells with cilia. Additionally, nonspecific protection can be achieved through the actions of the host's nonpathogenic microflora. If these nonspecific barriers to microorganism invasion are breached, other host interactions occur. Complement has many nonspecific actions that may be used to control invasion of microorganisms. PMLs are an additional line of defense the host has available in prevention of infection. These cells are responsible for intracellular killing of pathogens through the use of enzymatic and oxidative mechanisms. The mononuclear phagocyte system allows for elimination of foreign material and debris from the inflammatory reaction. Additionally, the macrophages process and present antigens to T lymphocytes. B lymphocytes differentiate to produce plasma cells, which produce specific antibodies aimed at the invading microorganism. T lymphocytes are involved in the killing of pathogenic microorganisms and in the production of powerful immune modulators known as lymphokines. Fever and inflammation also serve to stimulate reactions aimed at destroying and removing the pathogen from the host system. These factors all play an important role in prevention of disease transmission in a human host.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B C Muzyka. 1996. Host factors affecting disease transmission.. https://pubmed.ncbi.nlm.nih.gov/8641520/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Analysis of HLA class I specific antibodies in patients with failed allografts.

BACKGROUND: The goals of this study are first to determine the epitope specificity of donor specific antibody (DSA) in the serum of alloimmunized transplant patients with a failed renal graft; and second to understand the correlation between the development of DSA and nondonor specific antibody (NDSA). METHODS: The sera of 35 pretransplant panel reactive antibody (PRA)-negative patients with failed allografts were examined with single-antigen (SA) luminex beads to identify human leukocyte antigen (HLA)-A and -B antibodies. Potential HLA antibody epitopes were identified by using computer software and verified by absorption and elution from single-antigen cell lines. RESULTS: Twenty-seven patients developed donor-specific HLA-A and/or -B antibodies, while the remaining eight patients had only nondonor-specific HLA-A and/or -B antibodies. The DSA-positive patients also had a long list of NDSA. Sixty-eight percent of the reactions found in 27 recipients with DSA were attributable to 66 epitopes on the mismatched donor HLA molecule. All 39 NDSA in eight patients with only NDSA shared 17 epitopes within positive allele specificities. By absorption and elution using recombinant cell lines having a single HLA specificity, we confirmed the epitopes involved in three patients. CONCLUSION: Development of most NDSA in patients with failed allografts is likely due to sharing epitopes with DSA and/or other NDSA.

Antibody Formation↗

Human keratinocyte Toll-like receptors promote distinct immune responses.

It has been well established that Toll-like receptors (TLRs) are expressed by keratinocytes and respond to their respective ligands to initiate immune responses. However, it appears that keratinocytes, via differential activation of TLRs, may play a key role in determining the type of subsequent cutaneous immune response generated against a particular pathogen.

Antibody Formation↗