Lipopolysaccharide (LPS), a glycolipid found in the cell wall of Gram-negative bacteria, exerts pleiotropic biological effects in different cell types. LPS is mainly recognized by the Toll-like receptor (TLR) 4/MD2/Cluster of differentiation 14 complex (CD14). We previously demonstrated that LPS produced a direct action on thyroid cells, including up-regulation of thyroglobulin gene expression. This work aimed to study further the effect of LPS on thyroid function and to elucidate the mechanism by which LPS is recognized by the thyroid cell. We could detect the transcript and protein expression of TLR4, MD2, and CD14 in thyroid cells, and that these proteins are localized at the plasma membrane. The sodium iodide symporter (NIS) is the transporter involved in the iodide uptake, the first step in thyroid hormonogenesis. We demonstrated that LPS increases the TSH-induced iodide uptake and NIS protein expression. The LPS agonist lipid A reproduced LPS effect, whereas the LPS antagonist, polymyxin B, abrogated it. By the use of anti-TLR4 blocking antibodies and the transient expression of TLR4 dominant-negative forms, we evidenced the involvement of TLR4 in the LPS action. The enrichment of TLR4 expressing Fisher rat thyroid cell line-5 (FRTL-5) cells confirmed that TLR4 confers LPS responsiveness to thyroid cells. In conclusion, we revealed for the first time that all the components of the LPS receptor complex are expressed in thyroid cells. Evidence that the effects of LPS on rodent thyroid function involve TLR4-induced signaling was obtained. The fact that thyroid cells are able to recognize and respond to LPS supports a role of the endotoxin as a potential modifier of thyroid function.

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The effect of the pathogen Phytophthora austrocedrae on tree physiology of Austrocedrus chilensis in Patagonia was studied in a 4‐week study. In the first week, stem‐inoculated saplings showed a significant decrease in photosynthesis (A) without alteration of stomatal conductance (gs) or stem‐specific hydraulic conductivity (Ks). From the second week on, progressive decreases in A, gs and Ks were observed, concomitantly with development of significant stem lesions. Water use efficiency (WUE) increased in the second week and declined progressively from the third week. Hyphae and resinous materials were observed in tracheids and rays below lesions. Necrosis of parenchyma ray cells and blockage of tracheids torus were observed. Healthy xylem showed no resinous materials or tracheid blockage, but abundant starch in rays, which was absent in altered xylem. The culture filtrate (CF) of the pathogen was shown to induce changes in extracellular pH and conductivity, and increased necrosis in tissues of leaves and stem challenged with CF in vitro. Similar results were obtained in leaf tissues of the inoculated saplings in vivo. CF injection into xylem of saplings induced a decline in A and disturbance of leaf tissue integrity, without altering gs, WUE or Ks. The decrease of A correlated with changes in tissue integrity. A possible mechanism of A. chilensis decline induced by P. austrocedrae is discussed.