Chlamydophila psittaci (C. psittaci) is a human zoonotic pathogen, which could result in severe respiratory disease. In the present study, we investigated the role and mechanism of the type III secretion system (T3SS) of C. psittaci in regulating the inflammatory response in host cells. C. psittaci-infected THP-1 cells were incubated with the specific T3SS inhibitor INP0007, inhibitors of ERK, p38, or JNK, and the levels of inflammatory cytokines were analyzed using Q-PCR and ELISA. The levels of ERK, p38, and JNK phosphorylation were analyzed by Western blot. Our results verified that INP0007 inhibited chlamydial growth in vitro, but the coaddition of exogenous iron completely reversed the growth deficit. INP0007 inhibited the growth of C. psittaci and decreased the levels of IL-8, IL-6, TNF-α, and IL-1β. Exogenous iron restored the chlamydial growth but not the production of inflammatory cytokines. These results demonstrated that the expression of inflammatory cytokines during infection was associated with the T3SS which reduced by incubation with ERK and JNK inhibitors, but not with p38 inhibitor. We concluded that the T3SS elicited inflammatory responses by activating the JNK or ERK signaling pathways in the infection of C. psittaci.

Chlamydophila psittaci is an important intracellular pathogen. Persistent infection is an important state of the host-parasite interaction in this chlamydial infection, which plays a significant role in spreading the organism within animal populations and in causing chronic chlamydiosis and serious sequelae. In this study, a C. psittaci persistent infection cell model was induced by penicillin G, and real-time quantitative PCR was used to study the transcriptional levels of 10 C. psittaci genes (dnaA, dnaK, ftsW, ftsY, grpE, rpsD, incC, omcB, CPSIT_0846, and CPSIT_0042) in acute and penicillin-G-induced persistent infection cultures. Compared with the acute cultures, the penicillin-G-treated cultures showed a reduced chlamydial inclusion size and a significantly decreased number of elementary body particles. Additionally, some enlarged aberrant reticulate body particles were present in the penicillin- G-treated cultures but not the acute ones. The expression levels of genes encoding products for cell division (FtsW, FtsY) and outer membrane protein E encoding gene (CPSIT_0042) were downregulated (p < 0.05) from 6 h post-infection onward in the persistent infection cultures. Also from 6 h post-infection, the expression levels of DnaA, DnaK, IncC, RpsD, GrpE, and CPSIT_0846 were upregulated (p < 0.05); however, the expression level of OmcB in the persistent infection was almost the same as that in the acute infection (p > 0.05). These results provide new insight regarding molecular activities that accompany persistence of C. psittaci, which may play important roles in the pathogenesis of C. psittaci infection.

The obligate intracellular bacterium Chlamydia psittaci is the causative agent of psittacosis in birds and humans. The capability of this zoonotic pathogen to develop a persistent phase may serve a role in the chronicity of infections, in addition to the failure of antibiotic therapy or immunoprophylaxis. In the present study, a C. psittaci strain 6BC persistent infection cell model was induced using interferon (IFN)‑γ, alterations in the infectivity and morphology of the pathogen were analyzed, and the transcript profile of seven selected genes was analyzed. Following treatment with IFN‑γ, the infectivity of C. psittaci 6BC was decreased, the inclusion bodies appeared to be smaller, reticulate bodies were larger and the number of infectious elementary bodies was decreased compared with acute infection. In IFN‑γ‑induced persistently infected cells, the relative mRNA expression levels of the genes CPSIT‑0208, CPSIT‑0310, CPSIT‑0846, CPSIT‑0844 and CPSIT‑0594 were upregulated at 2‑48 h post‑infection (p.i.). The genes CPSIT‑0959 and CPSIT‑0057 were downregulated at 2‑36 h p.i. The results of the present study advanced the understanding of C. psittaci persistent infection and demonstrated a number of previously unknown alterations in chlamydial gene expression, which may provide novel targets to further analyze this particular host‑pathogen interaction.

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Background Pheochromocytoma is a neuroendocrine tumor that can overproduce catecholamines. Heart failure and Takotsubo Syndrome (TTS) caused by excessive catecholamines are uncommon pheochromocytoma complications. Case presentation A 27-year-old woman was referred to our center for further preoperative assessment and adrenalectomy. She came to the emergency ward with the typical symptoms of acute coronary syndrome and heart failure, including chest stuffiness, dyspnea, epigastric pain, and diaphoresis. The high level of 24-hour urinary vanillylmandelic acid and abdominal computed tomography findings supported the diagnosis of pheochromocytoma. Transthoracic echocardiography showed diffuse hypokinesis of the left ventricular wall with an ejection fraction of 23%. All symptoms and left ventricular function recovered rapidly after left laparoscopic adrenalectomy. Histopathology findings confirmed the diagnosis of pheochromocytoma. Based on the above findings, we eventually diagnosed her with pheochromocytoma-induced TTS. Conclusions This is a rare case of pheochromocytoma without hypertension complicated by TTS and acute heart failure. A diagnosis of pheochromocytoma-induced TTS should be considered for patients presenting with uncommon heart failure, even in patients without hypertension. Standard treatment is the surgical removal of the adrenal mass.