This possibility increased interest in the effect of chronic morphine use on the immune system. The first step of determining that morphine may affect the immune system was to establish that the opiate receptors known to be expressed on cells of the central nervous system are also expressed on cells of the immune system. One study successfully showed that dendritic cells, part of the innate immune system, display opiate receptors. Dendritic cells are responsible for producing cytokines, which are the tools for communication in the immune system. This same study showed that dendritic cells chronically treated with morphine during their differentiation produce more interleukin-12 (IL-12), a cytokine responsible for promoting the proliferation, growth, and differentiation of T-cells (another cell of the adaptive immune system) and less interleukin-10 (IL-10), a cytokine responsible for promoting a B-cell immune response (B cells produce antibodies to fight off infection).This regulation of cytokines appear to occur via the p38 MAPKs (mitogen-activated protein kinase)-dependent pathway. Usually, the p38 within the dendritic cell expresses TLR 4 (toll-like receptor 4), which is activated through the ligand LPS (lipopolysaccharide). This causes the p38 MAPK to be phosphorylated. This phosphorylation activates the p38 MAPK to begin producing IL-10 and IL-12. When the dendritic cells are chronically exposed to morphine during their differentiation process then treated with LPS, the production of cytokines is different. Once treated with morphine, the p38 MAPK does not produce IL-10, instead favoring production of IL-12.
Cefpodoxime is an oral, third-generation cephalosporin antibiotic. It is active against most Gram-positive and Gram-negative organisms. Notable exceptions include Pseudomonas aeruginosa, Enterococcus, and Bacteroides fragilis. Currently, it is only marketed as generic preparations in the US, according to the FDA Orange Book. It is commonly used to treat acute otitis media, pharyngitis, sinusitis, and gonorrhea. It also finds use as oral continuation therapy when intravenous cephalosporins (such as ceftriaxone) are no longer necessary for continued treatment. Cefpodoxime inhibits cell wall synthesis by inhibiting the final transpeptidation step of peptidoglycan synthesis in cell walls. It has well established pharmacokinetic profile with absorption of 50%. It is indicated in community acquired pneumonia, uncomplicated skin and skin structure infections, and uncomplicated urinary tract infections. It was patented in 1980 and approved for medical use in 1989. Spectrum of bacterial susceptibility and resistance
Cefpodoxime has been used to fight pathogenic bacteria responsible for causing gonorrhoea, tonsillitis, pneumonia, and bronchitis. Representative pathogenic genera include Streptococcus, Haemophilus, and Neisseria. The following represents MIC susceptibility data for a few medically significant microorganisms. Haemophilus influenzae: ≤0.03 – 1 μg/ml
Neisseria gonorrhoeae: 0.004 – 0.06 μg/ml
Streptococcus pyogenes: ≤0.004 – 2 μg/ml

Brand name
Zoetis markets cefpodoxime proxetil under the trade name  Simplicef for veterinary use, Finecure, India markets the products under trade name Cefpo.Vantin (by Pfizer) in suspension or tablet form.