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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

Corticotropin-releasing hormone accelerates log-phase growth of S. pneumoniae.S. pneumoniae, CRH exposed (2.1 × 10-4 μM/μl) vs. non-exposed, growth analysis was performed over a period of 9 h. Asterisks (∗) indicate significant (P ≤ 0.05) differences observed in the final bacterial mass during stationary phase. All experiments were performed in duplicates.
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Figure 3: Corticotropin-releasing hormone accelerates log-phase growth of S. pneumoniae.S. pneumoniae, CRH exposed (2.1 × 10-4 μM/μl) vs. non-exposed, growth analysis was performed over a period of 9 h. Asterisks (∗) indicate significant (P ≤ 0.05) differences observed in the final bacterial mass during stationary phase. All experiments were performed in duplicates.

Mentions: We compared the bacterial growth curve in presence and absence of CRH. A significant difference (P ≤ 0.05) was observed in bacteria exposed to CRH during log phase growth. In addition, significant differences in the final bacterial mass were observed during stationary growth phase (Figure 3).


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

Ndjom CG, Jones HP - Front Microbiol (2015)

Corticotropin-releasing hormone accelerates log-phase growth of S. pneumoniae.S. pneumoniae, CRH exposed (2.1 × 10-4 μM/μl) vs. non-exposed, growth analysis was performed over a period of 9 h. Asterisks (∗) indicate significant (P ≤ 0.05) differences observed in the final bacterial mass during stationary phase. All experiments were performed in duplicates.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Corticotropin-releasing hormone accelerates log-phase growth of S. pneumoniae.S. pneumoniae, CRH exposed (2.1 × 10-4 μM/μl) vs. non-exposed, growth analysis was performed over a period of 9 h. Asterisks (∗) indicate significant (P ≤ 0.05) differences observed in the final bacterial mass during stationary phase. All experiments were performed in duplicates.
Mentions: We compared the bacterial growth curve in presence and absence of CRH. A significant difference (P ≤ 0.05) was observed in bacteria exposed to CRH during log phase growth. In addition, significant differences in the final bacterial mass were observed during stationary growth phase (Figure 3).

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