In this report, we evaluated the effect of the pasteurization (P) process of mother's own milk (MOM) on the miRNA content of extracellular vesicles (EVs) and its impact on innate immune responses. Differences in size or particle number were not observed upon pasteurization of MOM (PMOM). However, significant differences were observed in the EV membrane marker CD63 and miRNA profiles. miRNA sequencing identified 33 differentially enriched miRNAs between MOM and PMOM. These changes correlated with significant decreases in the ability of PMOM to modulate IL-8 secretion in intestinal Caco2 cells where only MOM were able to decrease IL-8 secretion in presence of TNFα. While EVs from MOM and PMOM were both able to induce a tolerogenic M2-like phenotype in THP-1 macrophages, a significant decrease in the transcript levels of IL-10 and RNA sensing genes was observed with PMOM. Together, our data indicates that pasteurization of MOM impacts the integrity and functionality of MOM, decreasing its EVs-mediated immunomodulatory activity. This data provides biomarkers that may be utilized during the optimization of milk processing to preserve its bioactivity.
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http://dx.doi.org/10.1038/s41598-023-37310-x | DOI Listing |
Sci Rep
June 2023
Department of Microbiology and Cell Science, Genetics Institute, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, USA.
In this report, we evaluated the effect of the pasteurization (P) process of mother's own milk (MOM) on the miRNA content of extracellular vesicles (EVs) and its impact on innate immune responses. Differences in size or particle number were not observed upon pasteurization of MOM (PMOM). However, significant differences were observed in the EV membrane marker CD63 and miRNA profiles.
View Article and Find Full Text PDFPLoS One
May 2016
Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India; Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, India.
Transactivator protein C is required for the expression of bacteriophage Mu late genes from lys, I, P and mom promoters during lytic life cycle of the phage. The mechanism of transcription activation of mom gene by C protein is well understood. C activates transcription at Pmom by initial unwinding of the promoter DNA, thereby facilitating RNA polymerase (RNAP) recruitment.
View Article and Find Full Text PDFBiochemistry
March 2009
Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore 560012, India.
Transactivator protein C of bacteriophage mu is essential for the transition from middle to late gene expression during the phage life cycle. The unusual, multistep activation of mom promoter (P(mom)) by C protein involves activator-mediated promoter unwinding to recruit RNA polymerase and subsequent enhanced promoter clearance of the enzyme. To achieve this, C binds its site overlapping the -35 region of the mom promoter with a very high affinity, in Mg(2+)-dependent fashion.
View Article and Find Full Text PDFNucleic Acids Res
November 2008
Department of Molecular Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Lytic development of bacteriophage Mu is controlled by a regulatory cascade and involves three phases of transcription: early, middle and late. Late transcription requires the host RNA polymerase holoenzyme and a 16.5-kDa Mu-encoded activator protein C.
View Article and Find Full Text PDFProtein Eng Des Sel
January 2007
Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore 560 012, India.
Transcription activator protein C of bacteriophage Mu activates transcription of the late genes, including mom, during the lytic cycle of the phage. C binding to its site leads to the alteration in DNA topology of the promoter elements resulting in RNA polymerase (RNAP) recruitment. At the next step, the transactivator enhances promoter clearance of RNAP from P(mom).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!