The reason for their low content is unknown. Mice transgenic for a-defensins not dependent on C/EBP-e, e.g. the enteric human defensin 5 or 6, have shown expression levels comparable to human conditions as mice naturally express enteric a-defensins. An explanation for the low HNP-1 expression in the transgenic HNP-1 mouse could be lack of responsiveness to murine C/EBPe. To test this, we transduced human C/EBP-e into primary bone marrow cells of the transgenic HNP-1 mouse. Treatment with histone LEE011 deacetylase inhibitors might alleviate this inhibition. The integration site itself is another important factor which determines transgenic gene expression. Such positions effects are in general suppressive and more prominent if multiple nearly identical transcription factors are juxtaposed. Such phenomena may very well influence HNP-1 expression in the transgenic mouse in which approximately 20 bacterial artificial chromosome inserts, each containing 4 copies of DEFA1 as well as a truncated version of the DEFA3 gene, are integrated into a single chromosomal site. We have previously shown that unprocessed proHNP is primarily secreted into the bone marrow plasma, whereas fully processed HNP is retained in azurophil granules. Diminished posttranslational cleavage of proHNP could thus contribute to the shortage of HNPs observed in neutrophils of SGD patients. The enzymes responsible for posttranslational processing of proHNP are still not known and it is possible that these might be expressed under control of C/EBP-e albeit processing ceases when C/EBP-e expression is at its peak. We found intact posttranslational processing of HNP-1 by pulsechase biosynthesis, but diminished amounts by Western blotting. Infections remain a major cause of morbidity and mortality in the world especially in Low-and-Middle Income Countries. Antibiotics have been a significant force in reducing mortality in bacterial infections. However the number of effective antibiotics have been diminishing due to emerging bacterial resistance. Recently identified mechanisms of bacterial resistance such as New Delhi metallo-b-lactamase 1 may have grave consequences. Resistance is not only rapidly spreading in hospitals in the cities, but also in the community and in rural areas. The effectiveness of even life saving antibiotics have diminished with Escherichia coli resistance to ceftazidime and cefotaxime as high as 70% and 80% respectively in intensive care settings. Among the factors contributing to bacterial resistance, antibiotic consumption, both individual and aggregate, appear to have a major role. Irrational use of antibiotics is a factor in many countries such as India. In 2001, the WHO Strategy for Containment of Antimicrobial Resistance suggested steps to ensure rational use of antibiotics. One of the major strategies suggested was formulation of antibiotic stewardship programmes with development of antibiotic policy guidelines being a core component. The key purpose of guidelines is to improve rational antibiotic use.