Loss of Inorganic Ions from Host Cells Infected with Chlamydia psittaci

Abstract

Mouse fibroblasts (L cells) infected with the 6BC strain of Chlamydia psittaci released potassium ion (K + ) into the extracellular milieu in a way that depended on size of inoculum and time after infection. When the multiplicity of infection was 500 to 1,000 50% infectious units (ID 50 ) per L cell, loss of intracellular K + was first apparent 4 to 10 h after infection and was nearly complete at 6 to 20 h. Magnesium ion and inorganic phosphate (P i ) were also released. Similar multiplicities of ultraviolet-inactivated C. psittaci also caused release of K + . Leakage of inorganic ions probably resulted from immediate damage to the host-cell plasma membrane during ingestion of large numbers of chlamydiae. With multiplicities of 1 to 50 ID 50 per L cell, ingestion of C. psittaci was not by itself enough to cause release of K + and P i from infected L cells. There was a delay of 36 to 72 h between infection and massive leakage of intracellular ions during which time the chlamydiae multiplied extensively. Fifty ID 50 of ultraviolet-inactivated C. psittaci per L cell did not bring about significant leakage of K + , even after 72 h. The mechanism whereby these multiplicities of infection destroy the ability of host cells to retain intracellular molecules is not known. HeLa 229 cells also released K + and P i after infection, but these losses occurred more slowly than in comparably infected L cells, possibly because C. psittaci did not multiply as extensively in HeLa cells as it did in L cells. The significance of the inability of chlamydiae-infected cells to regulate the flow of molecules through their plasma membranes is discussed.

Chlamydia Uses K+ Electrical Signalling to Orchestrate Host Sensing, Inter-Bacterial Communication and Differentiation

“…In Chlamydia, although sequence homology suggests the presence of K + channels in the genome, the only role for K + demonstrated experimentally during the bacterial lifecycle is for the maturation of cytokines [20]. In parallel, a decrease in cytoplasmic [K + ] during infection using high multiplicities of infection (MOI) of C. psittaci (MOI = 100) has been shown at a late time point [21], although this was dependent on high bacterial load, since it was undetectable at MOI = 10 [21]. Therefore, the K + distribution and variation during Chlamydia infection remain unexplored.…”

Cytopathicity of Chlamydia is largely reproduced by expression of a single chlamydial protease

“…Infection with Chlamydia causes massive stress to the host cell, and cytolytic activity associated with Chlamydia infection has been described for more than 30 years ( Friis, 1972 ;Todd and Storz, 1975 ;Chang and Moulder, 1978 ;Wyrick et al, 1978 ). By electron microscopy, massive changes to organelles were noticed at later stages of infection, such as dilation and vacuolation of ER, distortion of mitochondria, and nuclear condensation ( Todd and Storz, 1975 ;Todd et al, 1976 ).…”

Isolation and characterization of phagosomes containing Chlamydia psittaci from L cells

“…However, killing the chlamydiae with UV light has no effect on their entry into host cells (6). When large numbers of chlamydiae enter a host cell, a lesion appears to be produced in its plasma membrane, and cytosol enzymes and inorganic ions leak out (9,51). Large chlamydial inocula quickly kill mice (34) and cells in culture (24,32) even before the chlamydiae have started to multiply.…”