This manuscript describes studies on the effects of overexpression of retinoic acid-inducible gene (RIG-1), a cytosolic pattern recognition receptor protein, on changes in lung cytokine, lung inflammatory cell counts and bronchoalveolar lavage protein content that accompany morbidity and mortality in mice exposed to cigarette smoke followed by infection with influenza PR8 virus. It is concluded that RIG-1 overexpression improves mortality in cigarette smoke exposed and influenza PR8 virus infected mice by restoring anti-viral and anti-inflammatory cytokine levels to levels found in wild type mice infected with virus, but not exposed to cigarette smoke.
Comments
1. Title – the title claims that RIG-1 is overexpressed, however the data indicates that RIG-1 expression in increased by less than 2-fold (Fig. 5 B, compare bar 1 with bar 5). The same conclusion can be drawn from Fig. 1. I. I wonder if this can be called overexpression? …show more content…
Abstract, conclusions – This section must be revised to indicate that the conclusions reflect studies with mice. As written, it could be mistaken for studies with human subjects. It is stated that cigarette smoke mediated RIG-1 suppression may be partially responsible for the increased morbidity and mortality of smokers (mice) exposed to IAV. Contrary to these conclusions, cigarette smoke alone or in combination with influenza infection did not significantly suppress RIG-1 protein levels [Fig. 5 B (bars 1-4), statistical significance not shown] raising doubts about the protective effects of RIG-1.
3. Fig. 1.I – Bright field micrographs should be included. Not all cells are expressing RIG-1 and SP-C (D, E, F) perhaps indicating that the cell populations are not pure or type II cells have undergone de-differentiation.
4. Fig. 1.II – The micrographs are not clear. It appears as though RIG-1 expression is less in TG mice infected with PR8. Also there is more staining for NP in TG mice than in WT mice infected with PR8. Any
Comments
1. Title – the title claims that RIG-1 is overexpressed, however the data indicates that RIG-1 expression in increased by less than 2-fold (Fig. 5 B, compare bar 1 with bar 5). The same conclusion can be drawn from Fig. 1. I. I wonder if this can be called overexpression? …show more content…
Abstract, conclusions – This section must be revised to indicate that the conclusions reflect studies with mice. As written, it could be mistaken for studies with human subjects. It is stated that cigarette smoke mediated RIG-1 suppression may be partially responsible for the increased morbidity and mortality of smokers (mice) exposed to IAV. Contrary to these conclusions, cigarette smoke alone or in combination with influenza infection did not significantly suppress RIG-1 protein levels [Fig. 5 B (bars 1-4), statistical significance not shown] raising doubts about the protective effects of RIG-1.
3. Fig. 1.I – Bright field micrographs should be included. Not all cells are expressing RIG-1 and SP-C (D, E, F) perhaps indicating that the cell populations are not pure or type II cells have undergone de-differentiation.
4. Fig. 1.II – The micrographs are not clear. It appears as though RIG-1 expression is less in TG mice infected with PR8. Also there is more staining for NP in TG mice than in WT mice infected with PR8. Any