Erythromycin reduces nasal inflammation by inhibiting immunoglobulin production, attenuating mucus secretion, and modulating cytokine expression

Allergic rhinitis (AR) and chronic rhinosinusitis (CRS) share some similar pathological mechanisms. In current study, we intend to investigate the impact of AR on CRS. In addition, we explored the efficacy of erythromycin (EM) treatment on CRS mice with or without AR (CRSwoAR, CRSwAR). Study subjects were divided into control, CRSwoAR, and CRSwAR groups. Experimental mice were divided similarly into control, CRSwoAR, and CRSwAR groups. In addition, CRS mice were treated with EM at 0.75, 7.5, or 75 mg/kg or with dexamethasone (Dex) at 1 mg/kg. In our results, allergy exacerbates inflammation that was evident in nasal histology and cytokine expression both in patients and in mice with CRS. Dex 1 mg/kg, EM 7.5 or 75 mg/kg treatments significantly inhibited serum IgE and IgG2a in CRS mice. EM-treated CRS mice had significantly elevated IL-10 levels and had a reversal of Th-1/Th-2 cytokine expression in nasal-associated lymphoid tissue. MUC5AC expressions were significantly reduced in the 7.5 or 75 mg/kg EM-treated mice compared with untreated mice. EM showed inhibitions on immunoglobulin production and mucus secretion stronger than Dex. We concluded that comorbid AR enhanced inflammation of CRS. EM and Dex treatments showed similar anti-inflammatory effects on CRS but through partly different mechanisms.

STUDIES ON THE NASAL HISTOLOGY OF EPIDEMIC INFLUENZA VIRUS INFECTION IN THE FERRET

A study has been made of the nasal histology in normal ferrets and in ferrets during and after infection with epidemic influenza virus. During the acute stage of infection the respiratory epithelium of the nasal mucous membrane undergoes necrosis with desquamation of the superficial cells and exudation into the air passages, and an inflammatory reaction occurs in the submucosa. Repair begins on the 4th day after infection, and from the 6th to the 14th day the respiratory area is covered successively by a transitional, a stratified squamous, and finally a stratified columnar epithelium. By the 21st day after infection the epithelium has been largely restored to normal but repair in the submucosa and cartilage is still in progress. The respiratory mucosa is substantially normal in structure 1 month after infection although minor abnormalities of cellular arrangement and type can still be distinguished.

STUDIES ON THE NASAL HISTOLOGY OF EPIDEMIC INFLUENZA VIRUS INFECTION IN THE FERRET

A study of the respiratory mucous membrane was made in the turbinates of ferrets which had received repeated inoculations of influenza virus. There was no evidence that persistent immunity is related to the presence of a structural modification of the respiratory epithelium. In fact, the respiratory epithelium in fully immune animals differs histologically only in minor respects from that of the normal, untreated ferret. On the other hand, a functional difference exists between the normal and the previously infected animals as evidenced by a marked acceleration of the repair process in the latter. Serological studies at the time of reinfection, 4 months or more after the previous attack, indicate that a relation exists between the height of antibody titer and resistance. The degree of immunity is probably a product of serological immunity and the rate of tissue repair. The implications of these studies to the problem of influenza in man are discussed.