Abstract
Filarial infections are tropical diseases caused by nematodes of the Onchocercidae family such as Mansonella perstans. The infective larvae (L3) are transmitted into the skin of vertebrate hosts by blood-feeding vectors. Many filarial species settle in the serous cavities including M. perstans in humans and L. sigmodontis, a well-established model of filariasis in mice. L. sigmodontis L3 migrate to the pleural cavity where they moult into L4 around day 9 and into male and female adult worms around day 30. Little is known of the early phase of the parasite life cycle, after the L3 is inoculated in the dermis by the vector and enters the afferent lymphatic vessels and before the moulting processes in the pleural cavity. Here we reveal a pulmonary phase associated with lung damage characterized by haemorrhages and granulomas suggesting L3 reach the lung via pulmonary capillaries and damage the endothelium and parenchyma by crossing them to enter the pleural cavity. This study also provides evidence for a transient inflammation in the lung characterized by a very early recruitment of neutrophils associated with high expression levels of S100A8 and S100A9 proteins.
Highlights
Blood-feeding vectors inject filarial infective larvae (L3) into the host skin during a blood meal
We present a sequential analysis of L3 infection from their inoculation to day 8 when they are settled in the pleural cavity, revealing the presence of L3 in the lung
Pulmonary damage including haemorrhages and granulomas is observed suggesting that L3 could migrate to the pulmonary circulation and capillaries from where they could exit the lung to reach the pleural cavity
Summary
Blood-feeding vectors inject filarial infective larvae (L3) into the host skin during a blood meal. Most of the filarial species migrate through the host’s body from the skin to their definitive niche, mainly the lymphatic system, the serous cavities, the cardiopulmonary system, or connective tissues [1]. Rodent models are helpful to investigate the migratory routes of L3 showing an early pulmonary phase for the human Brugia malayi, and for the main animal models of filariasis e.g. Brugia pahangi, Acanthocheilonema viteae and Litomosoides sigmodontis [2]. The latter is the sole filaria to undergo full development in immunocompetent BALB/c mice [3]. Both are considered as ‘derived filariae’ [6]
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