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CRH promotes S. pneumoniae growth in vitro and increases lung carriage in mice.

Ndjom CG, Jones HP - Front Microbiol (2015)

Bottom Line: The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae.We demonstrated that CRH promotes S. pneumoniae titer-dependent proliferation, as well as accelerates log-phase growth.Results also showed an increase in pneumococcal-associated virulence protein A virulence gene expression in response to CRH.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Medical Genetics, University of North Texas Health Science Center, Fort Worth, TX USA ; Center for Biotechnology Education, Krieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD USA.

ABSTRACT
Streptococcus pneumoniae (S. pneumoniae), a commensal across the nasal passages, is responsible for the majority of infectious pneumonia cases worldwide. Previous studies have shown that hormonal factors may be influential in regulating S. pneumoniae's transition from a non-pathogen to a pathogenic state. The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae. Mice were infected with CRH-treated S. pneumoniae via intranasal route, showing an increase in pulmonary bacterial burden. We also quantified S. pneumoniae's response to CRH through limited serial dilutions and growth curve analysis. We demonstrated that CRH promotes S. pneumoniae titer-dependent proliferation, as well as accelerates log-phase growth. Results also showed an increase in pneumococcal-associated virulence protein A virulence gene expression in response to CRH. These results demonstrate a role for CRH in S. pneumoniae pathogenicity, thus implicating CRH in mediating the transition of S. pneumoniae into a pathogenic state.

No MeSH data available.


Related in: MedlinePlus

Streptococcus pneumoniae adhesion and virulence factors increase in the presence of CRH. pavA gene expression was determined by quantitative realtime PCR analysis of S. pneumoniae’s mRNA exposed to CRH (N = 3). The analysis showed overexpression of the bacterium’s adhesion and virulence gene (pavA) when compared to control genes. Asterisks (∗) indicate significant (P ≤ 0.05) difference between CRH treated (CRH-Sp) and non-CRH treated (Sp) bacterial groups.
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Figure 4: Streptococcus pneumoniae adhesion and virulence factors increase in the presence of CRH. pavA gene expression was determined by quantitative realtime PCR analysis of S. pneumoniae’s mRNA exposed to CRH (N = 3). The analysis showed overexpression of the bacterium’s adhesion and virulence gene (pavA) when compared to control genes. Asterisks (∗) indicate significant (P ≤ 0.05) difference between CRH treated (CRH-Sp) and non-CRH treated (Sp) bacterial groups.

Mentions: PavA gene expression is found to modulate bacterial adhesion, invasion, and inflammation associated with septicemia (Pracht et al., 2005). Figure 4 demonstrates a significant (P ≤ 0.05) increase in pavA mRNA expression by S. pneumoniae exposed to CRH, compared to untreated controls as determined by quantitative realtime PCR.


CRH promotes S. pneumoniae growth in vitro and increases lung carriage in mice.

Ndjom CG, Jones HP - Front Microbiol (2015)

Streptococcus pneumoniae adhesion and virulence factors increase in the presence of CRH. pavA gene expression was determined by quantitative realtime PCR analysis of S. pneumoniae’s mRNA exposed to CRH (N = 3). The analysis showed overexpression of the bacterium’s adhesion and virulence gene (pavA) when compared to control genes. Asterisks (∗) indicate significant (P ≤ 0.05) difference between CRH treated (CRH-Sp) and non-CRH treated (Sp) bacterial groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4389549&req=5

Figure 4: Streptococcus pneumoniae adhesion and virulence factors increase in the presence of CRH. pavA gene expression was determined by quantitative realtime PCR analysis of S. pneumoniae’s mRNA exposed to CRH (N = 3). The analysis showed overexpression of the bacterium’s adhesion and virulence gene (pavA) when compared to control genes. Asterisks (∗) indicate significant (P ≤ 0.05) difference between CRH treated (CRH-Sp) and non-CRH treated (Sp) bacterial groups.
Mentions: PavA gene expression is found to modulate bacterial adhesion, invasion, and inflammation associated with septicemia (Pracht et al., 2005). Figure 4 demonstrates a significant (P ≤ 0.05) increase in pavA mRNA expression by S. pneumoniae exposed to CRH, compared to untreated controls as determined by quantitative realtime PCR.

Bottom Line: The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae.We demonstrated that CRH promotes S. pneumoniae titer-dependent proliferation, as well as accelerates log-phase growth.Results also showed an increase in pneumococcal-associated virulence protein A virulence gene expression in response to CRH.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Medical Genetics, University of North Texas Health Science Center, Fort Worth, TX USA ; Center for Biotechnology Education, Krieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD USA.

ABSTRACT
Streptococcus pneumoniae (S. pneumoniae), a commensal across the nasal passages, is responsible for the majority of infectious pneumonia cases worldwide. Previous studies have shown that hormonal factors may be influential in regulating S. pneumoniae's transition from a non-pathogen to a pathogenic state. The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae. Mice were infected with CRH-treated S. pneumoniae via intranasal route, showing an increase in pulmonary bacterial burden. We also quantified S. pneumoniae's response to CRH through limited serial dilutions and growth curve analysis. We demonstrated that CRH promotes S. pneumoniae titer-dependent proliferation, as well as accelerates log-phase growth. Results also showed an increase in pneumococcal-associated virulence protein A virulence gene expression in response to CRH. These results demonstrate a role for CRH in S. pneumoniae pathogenicity, thus implicating CRH in mediating the transition of S. pneumoniae into a pathogenic state.

No MeSH data available.


Related in: MedlinePlus