Rehydration does not affect pulmonary immune responses to influenza or susceptibility to secondary bacterial pneumonia

Introduction

In our murine model of influenza, significant weight loss occurs up to day 7 post-infection [1]. We sought to determine whether weight loss from influenza could be altered by rehydration and whether this affects pulmonary immune responses.

Methods

Adult BALB/c mice were infected with X31 (H3N2) influenza (1:80) via the intranasal route and randomized to intraperitoneal rehydration with 20 ml/kg compound sodium lactate (CSL), normal saline (NS) or no rehydration (NR) starting on day 3 following infection and continued for 4 days (n = 5/group). On day 7, mice were challenged with 1 × 10⁶ Streptococcus pneumoniae (serotype 2). Two further cohorts of mice were challenged with different doses of influenza and rehydrated from day 3 to 7 to investigate pulmonary immune responses in the absence of bacteria. Mice were infected with 1:80 (n = 10/group) influenza and rehydrated once daily or 1:60 (n = 5/group) influenza and rehydrated twice (1:60) daily with 20 ml/kg CSL or not. Daily weight, survival following secondary bacterial pneumonia, number of colony-forming units (48 hours after bacterial challenge) from peripheral blood, lung, and nasal wash and cellularity in lung compartments were measured.

Results

Rehydration did not affect weight loss following 1:80 influenza infection (naïve mice (+0.3 ± 0.4 g), influenza plus NR (-1.58 ± 0.4 g), influenza plus CSL (-1.1 ± 0.7 g) and influenza with NS (-1.3 ± 0.4 g)). A repeat experiment with CSL once daily or twice daily did not alter weight loss compared with NR (P > 0.05). Survival or CFU counts following bacterial pneumonia did not differ between the groups (P > 0.05). The total number or activational status of bronchoalveolar, lung macrophages/monocytes and lymphocytes was not affected by rehydration following influenza infection or 48 hours following bacterial pneumonia (P > 0.05; P < 0.05 vs naïve mice).

Conclusions

Rehydration does not affect immunity or pathophysiology in a murine influenza infection model. Assuming these results can be extrapolated to the clinical setting, our findings support the use of conservative fluid resuscitation strategies in patients with influenza.