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PmrA-mediated lipopolysaccharide sub...

Tamayo, Rita.

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PmrA-mediated lipopolysaccharide substitutions: Role in antimicrobial peptide resistance and virulence of Salmonella enterica serovar Typhimurium.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	PmrA-mediated lipopolysaccharide substitutions: Role in antimicrobial peptide resistance and virulence of Salmonella enterica serovar Typhimurium./
作者:	Tamayo, Rita.
面頁冊數:	215 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1146.
Contained By:	Dissertation Abstracts International65-03B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3126356
ISBN:	0496736426

PmrA-mediated lipopolysaccharide substitutions: Role in antimicrobial peptide resistance and virulence of Salmonella enterica serovar Typhimurium.
Tamayo, Rita.

PmrA-mediated lipopolysaccharide substitutions: Role in antimicrobial peptide resistance and virulence of Salmonella enterica serovar Typhimurium. - 215 p.

Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1146.

Thesis (Ph.D.)--The University of Texas Health Science Center at San Antonio, 2004.

Salmonella enterica serovar Typhimurium uses two-component regulatory systems (TCRS) to sense the extracellular environment and alter gene expression accordingly. The PhoP-PhoQ and PmrA-PmrB TCRS are induced in vivo and control the transcription of a large number of genes, including many that affect resistance to antimicrobial peptides (AP), central components of mammalian innate immunity. Several PhoP- or PmrA-activated genes increase AP resistance by affecting LPS structure such that the bacterium expresses poorer substrates for AP. PmrA-PmrB is required for production of aminoarabinose (Ara4N) and phosphoethanolamine (pEtN) modifications to LPS. The PmrA-activated genes necessary for Ara4N substitution have been characterized, however the PmrA-regulated genes involved in pEtN addition to LPS remain unknown.

ISBN: 0496736426Subjects--Topical Terms:

1017734
Biology, Microbiology.

PmrA-mediated lipopolysaccharide substitutions: Role in antimicrobial peptide resistance and virulence of Salmonella enterica serovar Typhimurium.
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245 1 0 $a PmrA-mediated lipopolysaccharide substitutions: Role in antimicrobial peptide resistance and virulence of Salmonella enterica serovar Typhimurium.
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500 $a Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1146.
500 $a Supervisor: John S. Gunn.
502 $a Thesis (Ph.D.)--The University of Texas Health Science Center at San Antonio, 2004.
520 $a Salmonella enterica serovar Typhimurium uses two-component regulatory systems (TCRS) to sense the extracellular environment and alter gene expression accordingly. The PhoP-PhoQ and PmrA-PmrB TCRS are induced in vivo and control the transcription of a large number of genes, including many that affect resistance to antimicrobial peptides (AP), central components of mammalian innate immunity. Several PhoP- or PmrA-activated genes increase AP resistance by affecting LPS structure such that the bacterium expresses poorer substrates for AP. PmrA-PmrB is required for production of aminoarabinose (Ara4N) and phosphoethanolamine (pEtN) modifications to LPS. The PmrA-activated genes necessary for Ara4N substitution have been characterized, however the PmrA-regulated genes involved in pEtN addition to LPS remain unknown.
520 $a This study identifies a number of new PmrA-activated genes and genes necessary for resistance to polymyxin B. Nine new PmrA-regulated genes not affecting AP resistance were identified, suggesting that PmrA controls phenotypes unrelated to AP resistance and virulence. The structures of LPS from PmrA-regulated gene mutants were analyzed for altered modifications, and two putative pEtN transferase gene mutants were identified. PmrC appears to be a lipid A-specific pEtN transferase; STM4118 may be involved in producing pEtN substitutions to core phosphates.
520 $a PmrA is essential for virulence in mice. The virulence defect of a pmrA (Ara4N-deficient) mutant occurs when administered orally, but not when inoculated intraperitoneally, indicating that the ability to modify LPS with Ara4N functions in survival of Salmonella early during infection, such as in the small intestine. Experiments were conducted to determine the role of PmrA-mediated LPS modifications in survival within specific microenvironments of the gastrointestinal tract and related immune tissues. While specific intestinal AP tested did not affect survival of Ara4N-deficient bacteria, different levels of a number of cytokines and other immune factors were elicited in mouse Peyer's patches at early time points of infection.
520 $a Identification and phenotypic characterization of PmrA-regulated genes and genes necessary for PM resistance, as well as the elucidation of the role of LPS modifications in Salmonella pathogenesis, has contributed to a better understanding of the mechanisms by which enteric bacteria counteract the mechanisms of host innate immunity.
590 $a School code: 0853.
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Health Sciences, Immunology. $3 1017716
650 4 $a Biology, Molecular. $3 1017719
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710 2 0 $a The University of Texas Health Science Center at San Antonio. $3 1030926
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